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عضویت

جستجوی مقالات مرتبط با کلیدواژه « pparγ » در نشریات گروه « پزشکی »

  • Ramin Lotfi*, Farhad Salari
    Background

    Designing the primer pairs is one of the most important factors in the amplification and quantitative analysis of the nucleic acid sequences of interest. Using in silico methods, the present study intends to design highly specific primers for quantitative analysis of the genes with minimum expression. To achieve this aim, we selected two candidate genes with little expression, namely, G-protein coupled receptor 120 (GPR120) and peroxisome proliferator-activated receptor-γ (PPARγ), in peripheral blood leukocytes of healthy volunteers.

    Methods

    Peripheral blood was collected from 30 healthy volunteers. Primers for GPR120 and PPARγ were designed using online websites (UCSC, OligoCalc, and OligoAnalyzer) and the primer designing tool (NCBI). Total RNA extraction and cDNA synthesis were done using commercially available kits based on manufacturer instructions. Finally, the melting curve analysis of GPR120 and PPARγ was assessed using the quantitative real-time PCR method.

    Results

    The in silico gene expression investigation revealed that GPR120 and PPARγ have minimal leukocyte expression. Besides, the melting curves analysis for both genes in the studied individuals showed only one melting peak, confirming the specific amplification of the desired genes.

    Conclusion

    Altogether, the study findings indicated that we could utilize the peripheral blood sample for assessing the gene expression and amplification of omega-3 fatty acids receptors, i.e. GPR120 and PPARγ as two candidate genes with very low expression in leukocytes.

    Keywords: GPR120, Omega-3 fatty acid, cDNA, PPARγ, Real-time PCR}
  • سیما نوری، سقا فرج تبار بهرستاق*
    سابقه و هدف

    فاکتور رونویسی Nrf2 تنظیم کننده اصلی پروتئین های آنتی اکسیدانی است و همراه با PPARγ در همه بافت های بدن بیان می شود. همچنین سیر با جلوگیری از غیرفعال شدن انسولین اثرات هیپوگلیسمی دارد. هدف از انجام پژوهش حاضر بررسی اثر تمرین مقاومتی همراه با مکمل سیر بر بیان ژن Nrf2 و PPARγ کبدی موش های صحرایی دیابتی بود.

    مواد و روش ها

    در مطالعه حاضر روش تحقیق از نوع تجربی بود. برای انجام تحقیق آزمایشگاهی حاضر 40 سر موش صحرایی نر ویستار پنج هفته ای با وزن 24‏‏‏‏‏‏‏‏‏/15 ± 12‏‏‏‏‏‏‏‏‏/162 گرم انتخاب و به طور تصادفی به پنج گروه کنترل-سالم (CN)، دیابت (DM)، دیابت-تمرین (DMT)، دیابت-سیر (DMG) و دیابت-تمرین-سیر (DMTG) تقسیم شدند. موش ها با تزریق نیکوتین آمید و بعد از 15 دقیقه تزریق STZ به صورت درون صفاقی دیابتی شدند. موش ها در گروه های مکمل 500 میلی گرم عصاره سیر به ازای هر کیلوگرم از وزن بدن با گاواژ دهانی به صورت روزانه دریافت کردند. تمرین مقاومتی روی نردبانی با شیب 80 درجه و با وزنه ای برابر 100-30 درصد وزن بدن انجام شد. جهت تجزیه و تحلیل استنباطی داده ها از آزمون تحلیل واریانس یک طرفه و آزمون تعقیبی توکی استفاده شد.

    یافته ها

    بیان Nrf2 افزایش معنی داری در گروه های دیابت-تمرین (022/0=p)، دیابت-سیر (029/0=p) و دیابت-تمرین-سیر (001/0=p) نسبت به دیابت؛ و دیابت-تمرین-سیر نسبت به گروه دیابت-تمرین (048/0=p) و دیابت-سیر (038/0=p) داشت. همچنین بیان PPARγ افزایش معنی داری در گروه های دیابت-تمرین (021/0=p)، دیابت-سیر (046/0=p) و دیابت-تمرین-سیر (006/0=p) نسبت به دیابت داشت.

    نتیجه گیری

    احتمالا مصرف عصاره سیر، تمرین مقاومتی و ترکیب تمرین مقاومتی با مکمل عصاره سیر از طریق تنظیم افزایشی Nrf2 و PPARγ موجب بهبود وضعیت آنتی اکسیدانی و کاهش فشار اکسایشی کبد می شود.

    کلید واژگان: تمرین مقاومتی, سیر, دیابت, Nrf2 و PPARγ}
    S .Noori, S. Farajtabar Behrestaq*
    Background and Objectives

     Nrf2 transcription factor is the major regulator of antioxidant proteins and is expressed with PPARγ in all tissues of the body. Furthermore, garlic includes hypoglycemic effects by preventing the inactivation of insulin. The aim of this study was to explain effects of resistance training with garlic supplementation on Nrf2 and PPARγ gene expression in streptozotocin-treated diabetic rats.

     Materials & Methods

    In the present study, study method was experimental. To carry out the present laboratory study, 40 5-w-old male Wistar rats weighing 162.12 g ±15.24 were selected and randomly divided into five control groups of healthy, diabetes, diabetes-exercise, diabetes-garlic and diabetes-exercise-garlic groups. Rats became diabetics by injecting nicotinamide and intraperitoneally injecting STZ after 15 min. Rats in the supplement groups received 500 mg of garlic extract per kilogram of the body weight daily by oral gavage. Resistance training was carried out on a ladder with a slope of 80° and with weights equal to 30–100% of the body weight. One-way analysis of variance and Tukey's post hoc test were used for inferential analysis of data.

    Results

    In general, Nrf2 expression significantly increased in diabetes-exercise (p = 0.022), diabetes-garlic (p = 0.029) and diabetes-exercise-garlic (p = 0.001) groups, compared to diabetic group; and diabetes-exercise-garlic compared to diabetes-exercise (p = 0.048) and diabetes-garlic group (p = 0.038). Expression of PPARγ increased significantly in diabetes-exercise (p = 0.021), diabetes-garlic (p = 0.046) and diabetes-exercise-garlic (p = 0.006) groups, compared to diabetic group.

    Conclusion

    Possibly, consumption of garlic extract, resistance training and a combination of resistance training with garlic extract supplement improve the antioxidant status and decrease the oxidative stress of the liver through the upregulation of Nrf2 and PPARγ.

    Keywords: Resistance training, Garlic, Diabetes, Nrf2, PPARγ}
  • سجاد اصغری وسطی کلائی، سقا فرج تبار بهرستاق*
    سابقه و هدف

    استرس اکسیداتیو به مقاومت به انسولین، اختلال عملکرد سلول های بتا و آسیب سلولی ناشی از هیپرگلیسمی کمک می کند که منجر به ایجاد دیابت شیرین می شود. هدف از پژوهش حاضر تبیین اثر تمرین هوازی و بربرین کلراید بر بیان ژن های UCP-1 و PPARγ بافت چربی احشایی موش های صحرایی دیابتی می باشد.

    مواد و روش ها

    در این مطالعه آزمایشگاهی، 32 موش صحرایی نر ویستار بالغ با وزن حدود 280-240 به طور تصادفی به چهار گروه (8=n): دیابت (DM)، دیابت-بربرین (DMB)، دیابت-تمرین هوازی (DMT)، دیابت-تمرین هوازی-بربرین (DMTB) تقسیم شدند. موش ها با تزریق mg/kg 60 STZ دیابتی شدند. موش هایی که قندخون آن ها بالاتر از mg/dl 300 بود به عنوان حیوانات دیابتی وارد تحقیق حاضر شدند. سپس گروه های تمرین به مدت شش هفته برنامه تمرین هوازی فزاینده (18-10 متر در دقیقه، 40-10 دقیقه در روز، پنج روز در هفته) را روی تردمیل انجام دادند. گروه مکمل نیز بربرین کلراید (mg/kg/day 30) یک بار در روز به صورت خوراکی با گاواژ دریافت کردند.

    یافته ها

    تجزیه و تحلیل داده ها نشان داد که اختلاف معنی داری در بیان ژن های UCP-1 (0/000=p) و PPARγ (0/002=p) در بین گروه ها وجود دارد. در ادامه نتایج نشان داد که بیان ژن UCP-1 در گروه دیابت-تمرین (1/85±2/96 و 0/015=p)، دیابت-بربرین کلراید 1/16±2/88 و 0/02=p) و دیابت-تمرین-بربرین کلراید (0/97±4/7 و 0/000=p) افزایش معنی داری نسبت به گروه دیابت داشت. همچنین بیان ژن PPARγ در گروه دیابت-تمرین-بربرین کلراید (0/36±1/6 و 0/002p=) افزایش معنی داری نسبت به گروه دیابت داشت.

    نتیجه گیری

    بر اساس نتایج این مطالعه، تمرین هوازی و بربرین کلراید یکی از راه های احتمالی مناسب برای جلوگیری از التهاب و آسیب های ناشی از دیابت می باشد.

    کلید واژگان: تمرین هوازی, بربرین کلراید, دیابت, UCP-1, Pparγ}
    S .Asghari Vostakolaei, S. Farajtabar Behrestaq*
    Background and Objective

    Oxidative stress contributes to insulin resistance, beta-cell dysfunction, and hyperglycemia-induced cellular damage, leading to diabetes mellitus. The purpose of this study is to explain the effect of aerobic exercise and berberine chloride on the expression of UCP-1 and PPARγ genes in the visceral fat tissue of diabetic rats.

    Methods

    In this laboratory study, 32 adult male Wistar rats weighing about 240-280 were randomly divided into four groups (n=8): diabetes (DM), diabetes-berberine (DMB), diabetes-aerobic exercise (DMT), diabetes-aerobic exercise-berberine (DMTB). The rats became diabetic by injecting 60 mg/kg STZ. The rats whose blood sugar was higher than 300 mg/dl were included in the present study as diabetic animals. The exercise groups then performed an incremental aerobic exercise program (10-18 m/min, 10-40 min/day, five days/week) on a treadmill for six weeks. The supplement group also received berberine chloride (30 mg/kg/day) orally by gavage once a day.

    Findings

    Data analysis showed that there is a significant difference in the expression of UCP-1 (p=0.000) and PPARγ (p=0.002) genes between the groups. Furthermore, the results showed that the expression of UCP-1 gene in the diabetes-exercise group (2.96±1.85 and p=0.015), diabetes-berberine chloride (2.88±1.16 and p=0.02) and diabetes-exercise-berberine chloride (4.7±0.97 and p=0.000) showed a significant increase compared to the diabetes group. Also, PPARγ gene expression in the diabetes-exercise-berberine chloride group (1.6±0.36 and p=0.002) showed a significant increase compared to the diabetes group.

    Conclusion

    According to the results of this study, aerobic exercise and berberine chloride is one of the possible ways to prevent inflammation and damage caused by diabetes.

    Keywords: Aerobic Exercise, Berberine Chloride, Diabetes, UCP-1, Pparγ}
  • Liqiang Chen, Yajuan Yin, Chunmiao Liu, Junying Liu, Mingqi Zheng, Yida Tang, Qing Yang, Jing Liu, Fan Chen, Lanbo Liu, Gang Liu *
    Objective(s)
    Bevacizumab is a commonly used anticancer drug in clinical practice, but it often leads to adverse reactions such as vascular endothelial damage, hypertension, arterial and venous thrombosis, and bleeding. This study investigated the protective effects of metformin against bevacizumab-induced vascular injury in a mouse model and examined the possible involvement of GDF15/PI3K/AKT/FOXO/PPARγ signaling in the effects.
    Materials and Methods
    C57 male mice were purchased. To investigate metformin, the mice were assigned to the saline, bevacizumab (15 mg every 3 days), metformin (1200 mg/day), and bevacizumab+metformin groups. To investigate GDF15, the mice were assigned to the siNC+bevacizumab, siNC+bevacizumab+metformin, siGDF15+bevacizumab, and siGDF15+bevacizumab+metformin groups. Histological staining was used to evaluate vascular injury. Flow cytometry was used to evaluate apoptosis. ELISA was used to measure plasma endothelial injury markers and proinflammatory cytokines. qRT-PCR and western blot were used to determine the expression of GDF15 and PI3K/AKT/FOXO/PPARγ in aortic tissues.
    Results
    Metformin alleviated bevacizumab-induced abdominal aortic injury, endothelial cell apoptosis, and systemic inflammation in mice (all P<0.05). Metformin up-regulated GDF15 expression and PI3K/AKT/FOXO/PPARγ signaling in the abdominal aorta of mice treated with bevacizumab (all P<0.05). siGDF15 abolished the vascular protective and anti-inflammatory effects of metformin (all P<0.05). siGDF15 suppressed PI3K/AKT/FOXO/PPARγ signaling in the abdominal aorta of mice treated with bevacizumab (all P<0.05).
    Conclusion
    Metformin attenuates bevacizumab-induced vascular endothelial injury, apoptosis, and systemic inflammation by activating GDF15/PI3K/AKT/FOXO/PPARγ signaling.
    Keywords: Bevacizumab, Growth differentiation-factor 15, Metformin, Mouse, PI3K, AKT, FOXO, PPARγ-, Signaling pathway, Vascular injuries}
  • مهدی زارعی*، زینب کدخدا، علی یعقوبی
    مقدمه

    اصلاح سبک زندگی از طریق تغییر رژیم غذایی به همراه تمرین ورزشی رویکرد اصلی در درمان کبد چرب غیرالکلی است. هدف از این پژوهش بررسی تاثیر تمرین تناوبی شدید همراه با مصرف مکمل خرفه بر گیرنده X کبدی آلفا (LXRα) و گیرنده گاما فعال کننده تکثیر پروکسی زوم (PPARγ) در کبد موش های صحرایی مبتلا به کبد چرب غیرالکلی بود.

    مواد و روش ها

    در این مطالعه تجربی، 30 سرموش صحرایی نر از نژاد ویستار؛ با دامنه وزنی 185-160 گرم، به دو گروه اصلی بیمار (25=n) و شاهد سالم (5=n) تقسیم شدند. کبد چرب غیرالکلی با 12 هفته رژیم غذایی پرچرب القاء شد. پنج موش برای تایید ابتلا قربانی شدند و مابقی موش ها به چهار زیرگروه پنج تایی شامل شاهد کبد چرب، مکمل خرفه، تمرین و تمرین+مکمل خرفه تقسیم شدند. مکمل یاری با خرفه شامل دریافت روزانه 400 میلی گرم بر کیلوگرم وزن بدن پودر حل شده خرفه بود. تمرین تناوبی شدید شامل 5 جلسه در هفته دویدن با شدت 90 درصد سرعت بیشینه به مدت 8 هفته بود. در پایان، مقادیر LXRα و PPARγ بافت کبد اندازه گیری شد.

    یافته ها

    مقادیر LXRα در گروه های تمرین+مکمل (0/002=p، اندازه اثر=0/63)، تمرین (0/017=p، اندازه اثر=0/43) و مکمل (0/009=p، اندازه اثر=0/44) در مقایسه با گروه شاهد کبدچرب به طور معناداری پایین تر بود. مقادیر LXRα در گروه تمرین+مکمل به طور معناداری نسبت به گروه تمرین (0/030=p) و گروه مکمل (0/030=p) پایین تر بود. مقادیر PPARγ در گروه های تمرین+مکمل (0/002=p، اندازه اثر=0/83)، تمرین (0/030=p، اندازه اثر=0/60) و مکمل (0/004=p، اندازه اثر=0/71) نسبت به گروه شاهد کبد چرب به طور معناداری پایین تر بود. مقادیر PPARγ در گروه تمرین+مکمل به طور معناداری (0/030=p) نسبت به گروه تمرین پایین تر بود.

    نتیجه گیری

     تمرین ورزشی تناوبی شدید به همراه مصرف مکمل خرفه ممکن است از طریق کاهش LXRα و PPARγ کبدی و بهبود تنظیم مسیرهای تولید چربی در کبد، در درمان بیماری کبد چرب غیر الکلی موثر باشد.

    کلید واژگان: تمرین تناوبی با شدت بالا, خرفه, بیماری کبد چرب غیر الکلی, آلفا LXR و گاما PPAR}
    M. Zarei*, Z .Kadkhoda, A .Yaghoubi
    Introduction

    Lifestyle modification through dietary interventions and exercise training is the main approach to treating nonalcoholic fatty liver (NAFLD). The aim of this study was to investigate the effect of high-intensity interval training (HIIT) with Portulaca oleracea supplementation on liver X receptor α (LXRα) and peroxisome proliferator-activated receptor γ (PPARγ) in the liver tissue of rats with NAFLD.

    Materials and Methods

    In this experimental study, 30 male rats with a weight range of 160-185 g were divided into 2 main groups: NAFLD (n=25) and healthy control (n=5). Nonalcoholic fatty liver was induced in rats with 12 weeks of a high-fat diet. Five rats were sacrificed to confirm the establishment of NAFLD, and the remaining rats were divided into 4 subgroups: fatty liver control (n=5), P. oleracea supplement (n=5), HIIT (n=5), and HIIT+P. oleracea supplement (n=5). Rats in supplementation groups were given 400 mg/kg/day of dissolved P. oleracea powder. HITT consisted of 5 sessions a week of running with an intensity of 90% of maximum speed for 8 weeks. At the end of the study, LXRα and PPARγ ​​levels in liver were measured.

    Results

    LXRα values were significantly lower in the HIIT+P. oleracea (P=0.002, effect size=0.63), HIIT (P=0.017, effect size=0.43), and P. oleracea groups (P=0.009, effect size=0.44) than in the fatty liver control group. LXRα values were significantly lower in the HIIT+P. oleracea group than in the HIIT (P=0.030) and P. oleracea groups (P=0.030). PPARγ values were significantly lower in the HIIT+P. oleracea (P=0.002, effect size=0.83), HIIT (P=0.030, effect size=0.60), and P. oleracea groups (P=0.004, effect size=0.71) than in the fatty liver control group. PPARγ values were significantly lower in the HIIT+P. oleracea group than in the HIIT group (P=0.030).

    Conclusion

    HIIT with P. oleracea supplementation may be effective in the treatment of NAFLD disease by reducing LXRα and PPARγ and improving the regulation of fat production pathways in the liver.

    Keywords: High-intensity interval training, Portulaca, Nonalcoholic fatty liver disease, LXRα, PPARγ}
  • Ebrahim Khaki, Khosro Jalali Dehkordi*, Farzaneh Taghian, Seyed Ali Hoseini
    Background and aims

    The consumption of grape seed nanoparticles extract can control cardiovascular risk factors. Exercise plays a protective role against cardiovascular disease. Therefore, the aim of the present study was to investigate the effect of eight-week resistance training (RT) and the use of grape seed nanoparticles on mitochondrial biogenesis of heart tissue in myocardial infarction (MI) models.

    Methods

    In this experimental study, 25 rats were randomly divided into five groups including (1) control (C), (2) MI, (3) MI+RT, (4) MI+grape seed, and (5) MI+RT+grape seed. MI was induced by subcutaneous injection of isoprenaline (85 mg/kg). Grape seed nanoparticles were daily administered at a dose of 150 mg/kg for 8 weeks, and RT was performed 5 days a week. Finally, data were analyzed using the one-way analysis of variance (ANOVA) and Tukey’s post hoc tests (P≤0.05).

    Results

    MI models showed decreased expression of PGC-1α, PPARγ, and UCP-1 genes in cardiac tissue (P=0.001). However, RT combined with the use of grape seed nanoparticles had a significant effect on increasing the expression of PGC-1α (P=0.001), PPARγ (P=0.002), and UCP-1 (P=0.003) genes in the heart tissue of MI model mice.

    Conclusion

    The consumption of grape seed nanoparticles along with RT has more effects on improving the expression of PGC-1α, PPARγ, and UCP-1 genes in MI than either alone. Therefore, the use of grape seed nanoparticles together with RT is recommended in case of MI.

    Keywords: Resistance Training, Grape seed, PGC-1α, PPARγ, UCP-1, Myocardial infarction}
  • Seyedeh Marzieh Moosavi, Abbas Akhavan Sepahi, Seyed Fazlollah Mousavi, Farzam Vaziri, Seyed Davar Siadat*
    Introduction

    Faecalibacterium prausnitzii is an important member of human gut microbiota with a critical function in the health of humans through the induction of inflammatory and immune responses leading to intestinal hemostasis. Microbiota-induced extracellular vesicles (EVs) were presented as a novel communication pathway between microbiota and the host that are capable of imposing positive effects on the host. Recently, EV-based treatments have been evaluated in different studies, and using EVs derived from microbiota has been recommended in recent studies as post-vaccination adjuvants. Accordingly, in the present study, the effects of various EV concentrations on the mRNA expression of peroxisome proliferator-activated receptor γ (PPARγ) and fasting-induced adipose factor (FIAF) genes were evaluated and optimized in the human epithelial colorectal adenocarcinoma (Caco-2) cell line.

    Methods

    The effects of the extracted EVs from F. prausnitzii on the PPARγ and FIAF gene expression were investigated in the Caco-2 cell line via cell culture and quantitative real-time PCR. The obtained outcomes were then compared with those of our previous study (concentrations of 50 and 100 µg/ml).

    Results

    It was shown that F. prausnitzii EVs (150 µg/ml) significantly increased PPARγ and FIAF gene expression in the Caco-2 cell line, relative to previous studies conducted by our team.

    Conclusion

    Considering the positive impact of F. Prausnitzii EVs on the studied genes’ expression in the present study, the EVs of the bacterium will be proposed as new post-vaccination adjuvants in people suffering from intestinal barrier disorders such as inflammatory bowel disease patients. However, more studies should be performed in this respect.

    Keywords: F. prausnitzii, EVs, PPARγ, FIAF, Caco-2 cell line}
  • Mingxiao Wen, Wenjun Chen, Qun Zhou, Xiaoqing Dou *
    Objective(s)
    Astragaloside IV (AS-IV) is a bioactive saponin with a wide range of pharmacological effects. This study was aimed at investigating its potential effect on polycystic ovary syndrome (PCOS). 
    Materials and Methods
    Female Sprague-Dawley rats were randomly divided into five groups (control, PCOS, PCOS+AS-IV 20 mg/kg, PCOS+AS-IV 40 mg/kg, and PCOS+AS-IV 80 mg/kg). The pathological injury level of rat ovary was observed with hematoxylin-eosin (H&E) staining; enzyme-linked immunosorbent assay (ELISA) kit was utilized to measure the levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone in rat serum; western blot detected autophagy-associated or peroxisome proliferator-activated receptor γ (PPARγ) pathway-related protein expression; immunofluorescence was performed to observe LC3 level in rat ovarian tissue. After co-treatment with AS-IV and PPARγ inhibitor, the proliferation in ovarian granulosa cell line KGN was examined employing cell counting kit-8 (CCK-8), EdU staining, and colony formation; cell apoptosis was observed with TdT-mediated dUTP nick-end labeling (TUNEL); apoptosis-related protein expression was assayed by western blot. 
    Results
    Treatment with AS-IV inhibited the ovarian pathological damage in PCOS rats. It also promoted the level of autophagy and activated PPARγ signaling in the rat PCOS model. In KGN cells, the level of autophagy and expression of PPARγ-related proteins were also elevated by AS-IV treatment. Furthermore, AS-IV facilitated autophagy, thus inhibiting KGN cell proliferation and promoting its apoptosis, through activating the PPARγ signaling pathway. 
    Conclusion
    AS-IV-activated PPARγ inhibits proliferation and promotes the apoptosis of ovarian granulosa cells, enhancing ovarian function in rats with PCOS.
    Keywords: Apoptosis, Astragaloside IV, Autophagy, Polycystic ovary syndrome, PPARγ, Rat}
  • Sepideh babaei garmkhani, Homayoun Khazali*
    Introduction

    Orexin A and adiponectin are involved in controlling metabolism and energy distribution in the body during lactation. Lactation is a process with high demand for lipid synthesis. Peroxisome proliferator-activated receptor gamma (PPARγ) and sterol regulatory element-binding protein 1 (SREBP1c) are two transcription factors that regulate milk lipid synthesis. The goal of this study was to assess the effects of mammary administration of the orexin A receptor antagonist on the expression of PPARγ and SREBP1c genes as well as serum adiponectin levels in the lactating rats.

    Methods

    Orexin A receptor antagonist (SB-334867) was injected intraductal into the mammary glands of lactating female rats at three doses of 1, 2 and 4 μg/kg BW in a solvent volume of 50 μL. The gene expressions of PPARγ and SREBP1c were measured using real-time polymerase chain reaction (PCR), along with serum levels of adiponectin using ELISA.

    Results

    The results of quantitative RT-PCR showed a significant decrease in the relative expression of PPARγ and SREBP1c genes compared to that of the control group. The rate of reduction at a dose of 4 µg/kg BW SB was greater than the doses of 1 and 2 µg/kg BW SB-334867. The serum levels of adiponectin significantly decreased in the 4 µg/kg BW SB group compared to that of the control group.

    Conclusion

    These results indicated that intra-mammary administration of 4 µg/kg orexin-A antagonist in lactating rats decreased the gene expression of two transcription factors involved in milk fat synthesis, accompanying by a reduction in serum adiponectin level.

    Keywords: Orexin antagonist, PPARγ, SREBP1, Adiponectin, Lactation}
  • Cordelia John, Sumathy Arockiasamy *
    Objective (s)

    In this study, we tested the hypothesis that sinapic acid (SA), a naturally occurring hydroxycinnamic acid found in vegetables, cereal grains, and oilseed crops with various biological activities suppresses adipogenesis in 3T3-L1 adipocytes by down-regulating adipogenesis transcription factor. 

    Materials and Methods

    3T3-L1 adipocytes were treated with SA and evaluated by Oil Red O staining, triglyceride estimation, lipolysis, and reverse transcription-polymerase chain reaction. 3T3-L1 adipocytes were treated with various concentrations of SA (100 to 1000 μmol) during differentiation. 

    Results

    SA prevented an increase in adipocytes by reducing preadipocyte clonal expansion. ORO staining analyses revealed that SA reduced cytoplasmic lipid droplet accumulation in 3T3-L1 by 57% at the highest concentration of 1000 μmol without affecting cell viability. Furthermore, SA down-regulated the expression of peroxisome proliferator-activated receptor-gamma, CCAAT/enhancer-binding protein alpha, sterol regulatory element-binding protein 1c, and fatty acid synthase. ROS generated during adipogenesis was also attenuated by SA treatment by increasing antioxidant enzymes superoxide dismutase, catalase, and the cellular antioxidant glutathione. SA demonstrated no in vivo toxicity in the Drosophila melanogaster model. 

    Conclusion

    These results suggest that SA exerts anti-oxidant and anti-adipogenic effects and could be used as a functional nutraceutical ingredient in combatting obesity-related diseases.

    Keywords: 3T3-L1 adipocytes, Adipogenesis, Fas, PPARγ, ROS, Sinapic acid}
  • Vijay Patil, Neha Upadhyay, Kalpana Tilekar, Hardik Joshi, Ramaa C S*
    Thiazolidinedione (TZD), being a privileged scaffold, has been known as a significant structural moiety of antidiabetic drugs. TZD has been known to improve glycaemic control in type 2 diabetes mellitus (T2DM) by increasing insulin sensitivity in the body. A novel series of 5-benzylidene 2,4-thiazolidinedione derivatives were designed, synthesized (V1-V28), and structurally confirmed by different spectroscopic techniques such as FTIR, 1H NMR, 13C NMR, and Mass spectrometry. Upon the safety assessment of the synthesized molecules in non-transformed hepatocytes by MTT reduction assay, these were found non-toxic. These derivatives were then further evaluated for their antihyperglycemic and antihyperlipidemic properties in a high-fat diet and low dose of streptozotocin-induced diabetic rats. Altogether, seven biochemical parameters were analyzed, namely blood glucose, triglycerides, cholesterol, creatinine, blood urea nitrogen, HDL-cholesterol, and glycosylated hemoglobin in serum by standard methods. Four synthetic molecules (V2, V4, V5, and V20) possessed significant hypoglycaemic and hypolipidemic activity as compared to the positive control pioglitazone. Moreover, the histopathological studies of the heart and liver revealed no significant toxicity. Two representative compounds V2 and V4, were evaluated for their PPARγ activation potential, demonstrating that they were partial PPARγ agonists, thus confirming our designing hypothesis. Based on the results obtained, we assume that these compounds have the potential to be developed as future antidiabetic agents.
    Keywords: Diabetes, Hypoglycaemic, Hypolipidemic, PPARγ, thiazolidinediones}
  • Aline Nassar, Maha Khachab, Hayat Zaatiti, Amjad Kanaan *
    Background

     Polycystic ovary syndrome (PCOS) is a prevalent reproductive and metabolic disorder. Insulin resistance (IR) is highly associated with PCOS and aggravates its symptoms. Thiazolidinediones (TZDs), as insulin sensitizing agents, are PPARγ agonists that improve many of the symptoms of PCOS. The Magnolia officinalis extract (MOE) is a natural peroxisome proliferator activated receptor gamma (PPARγ) agonist that improves insulin sensitivity in experimental models.

    Objectives

     Using a dehydroepiandrosterone (DHEA)-induced rat model of PCOS and IR, this study aimed to explore both the potential beneficial effects and the molecular mechanisms of action of MOE.

    Methods

     Post-pubertal female Sprague Dawley rats were subcutaneously injected daily with DHEA (6 mg/100 g body weight) dissolved in sesame oil for 28 days (n = 30). Age- and weight-matched control rats received only sesame oil (n = 12). Afterward, 16 of the DHEA-injected rats, along with five control rats, were sacrificed for blood and tissue collection. The 14 remaining DHEA-injected rats received either treatment of 30 days of oral MOE (500 mg/kg) dissolved in dimethyl sulfoxide (DMSO) (n = 7), or oral DMSO only (n = 7). Meanwhile, the remaining control rats (n = 7) continued to receive daily oral DMSO for 30 days. At the end of the treatments, the rats were sacrificed for blood and tissue collection.

    Results

     After 28 days, the DHEA-treated rats exhibited an increase in body weight as compared to controls (P < 0.05). DHEA injection induced a PCOS phenotype as evident by a statistically significant (P < 0.05) elevated serum luteinizing hormone (LH), and an increased number of cystically dilated follicles with thicker granulosa compared to controls. PCOS rats showed a statistically significant rise in fasting insulin with an increased homeostatic model assessment index of insulin resistance (HOMA-IR) as compared to controls (P < 0.05). Compared to the control group, PCOS rats had a statistically significant lower ovarian protein expression of PPARγ, insulin receptor substrate 1 (IRS1), and protein kinase B (Akt) by Western Blot (P < 0.05). Conversely, the PCOS group showed an increased mammalian target of rapamycin (mTOR) pathway activity as evident by an increase in the fraction of phosphorylated mTOR to total mTOR compared to the control group (P < 0.05). When treated for 30 days with oral MOE (500 mg/kg), the PCOS rats showed a statistically significant decrease in body weight and serum LH levels as compared to the non-treated PCOS rats (P < 0.05). The number of cystically dilated follicles in the MOE-treated PCOS rats was significantly reduced compared to the non-treated PCOS rats. In the MOE-treated PCOS rats, the ovarian protein expression of PPARγ, IRS1, and Akt was significantly increased, while the p-mTOR/mTOR expression was decreased compared to the non-treated PCOS group (P < 0.05).

    Conclusions

     According to our results, the MOE ameliorated the DHEA-induced PCOS phenotype histologically, hormonally, and metabolically. Fundamentally, this explores the elusive pathophysiologic association between IR and PCOS by targeting pathways common to both disorders.

    Keywords: PI3Kinase, PPARγ, Magnolia officinalis, Insulin Resistance, Polycystic Ovary Syndrome, mTOR}
  • مژگان صحرائی، احمد عبدی*، حامد جلال
    زمینه و هدف

    افزایش شیوع بیماری های متابولیک (مثل: دیابت و چاقی) به طور جدی سلامت انسان و ایمنی زندگی را در سراسر جهان تحت تاثیر قرار داده است. یافتن داروهای موثر با ترکیبات طبیعی و فعالیت ورزشی برای درمان بیماری های متابولیک از اهمیت بالایی برخوردار است. هدف از پژوهش حاضر بررسی اثر مصرف بربرین کلراید با تمرین هوازی بر بیان ژن Nrf2، HO-1 و PPARγ کبدی موش های صحرایی دیابتی با استرپتوزوتوسین (STZ) می باشد.

    روش کار

    در این مطالعه تجربی، 32 موش صحرایی نر ویستار به طور تصادفی به چهار گروه (8=n): دیابت (DM)، دیابت-بربرین (BDM)، دیابت- تمرین هوازی (TDM)، دیابت- تمرین هوازی- بربرین (TBDM) تقسیم شدند. دیابت با تزریق STZ در موش های نر القا شد. بربرین کلراید (mg/kg/day 30) یک بار در روز به صورت خوراکی با گاواژ خورانده شد. گروه های تمرین به مدت شش هفته برنامه تمرین هوازی فزاینده (18-10 متر در دقیقه، 40-10 دقیقه در روز، پنج روز در هفته) را روی تردمیل انجام دادند.

    یافته ها

    بیان Nrf2 و HO-1 در گروه های BDM (به ترتیب =0.027p و  p= 0.038)، TDM (به ترتیب  p=0.022 و  p=0.028) و TBDM (به ترتیب p=0.000 و p=0.000) افزایش معنی داری داشت. این افزایش در گروه های TBDM نسبت به BDM (به ترتیب  p=0.034 و  p=0.034) و TDM (به ترتیب p=0.043 و p=0.046) نیز مشاهده شد. PPARγ در گروه های TDM (p=0.046) و TBDM (p=0.001) افزایش معنی داری داشت.

    نتیجه گیری

    بربرین کلراید همراه با فعالیت ورزشی احتمالا از طریق تنظیم افزایشی مسیر Nrf2/HO-1 و PPARγ می تواند آسیب کبدی ناشی از STZ را مهار کند.

    کلید واژگان: فعالیت ورزشی, بربرین کلراید, Nrf2, PPARγ, دیابت}
    Mozhgan Sahraei, Ahmad Abdi*, Hamed Jalal
    Background & objectives

    The increased incidence of metabolic diseases (e.g., diabetes and obesity) has seriously affected human health and life safety worldwide. It is of great significance to find effective drugs from natural compounds and exercise to treat metabolic diseases. The aim of this study was to evaluate the effect of berberine chloride with aerobic training on Liver Gene Expression Nrf2, HO-1 and PPARγ in Streptozotocin (STZ)-induced diabetic rats.

     Methods

    In this experimental study,  32 male Wistar rats were randomly divided into four groups (n=8): Diabetes (DM), Diabetes-Berberine (BDM), Diabetes-Aerobic Training (TDM), Diabetes-Aerobic Training -Berberine (TBDM). Diabetes was induced by injection of STZ in male rats. Berberine chloride (30 mg/kg/day) were administered orally, by gavage, once a day. Training groups have performed a progressive aerobic running program (at 10-18 m/min, 10-40 min/day, and 5 days/week) on a motor-driven treadmill for six weeks.

    Results

    There was a significant increase in Nrf2 and HO-1 expression in BDM in BDM (p=0.027 and p=0.038, respectively), TDM (p=0.022 and p=0.028, respectively) and TBDM (p=0.000 and p=0.000, respectively). This increase was also observed in TBDM groups compared to BDM (p=0.034 and p=0.034, respectively) and TDM (p=0.043 and p=0.046, respectively). PPARγ was significantly increased in TDM (p=0.046) and TBDM (p=0.001) groups.

    Conclusions

    Berberine chloride combination with exercise may possibly inhibit STZ-induced liver damage through up-regulating the Nrf2/HO-1 pathway and PPARγ.

    Keywords: Exercise, Berberine Chloride, Nrf2, PPARγ, Diabetes}
  • Saeedeh Moinaldini, Mostafa Allahyari, Beydolah Shahouzehi, Hossein Fallah *
    Background
    The worldwide prevalence of diabetes is increasing. Diabetes is a complex disease that results from impaired secretion of insulin or insulin resistance. In adipose tissue, insulin increases glucose uptake by stimulating the transfer of glucose transporter type 4 (GLUT-4) to the plasma membrane. In this study, the effect of IRAK inhibitor (IRAKi) and pioglitazone on genes expression in adipose tissue of insulin resistant mice was evaluated.
    Methods
    Mice were randomly divided into 6 groups (n= 8 each), five groups of which were fed a high-fat diet and one group received a normal diet for 12 weeks. The treatment with pioglitazone and IRAKi was performed for 2 weeks. At the end of the study, the animals were sacrificed and the adipose tissue and blood samples were collected. The expression of GLUT4, TNF-α, peroxisome proliferator-activated receptor gamma (PPARγ), and Lepin were determined by real-time PCR in the adipose tissue. The malondialdehyde (MDA) level and total antioxidant capacity (TAC) in serum were measured. Results were analyzed by SPSS 22.
    Results
    The data showed that the combination of IRAKi and pioglitazone increased PPARγ expression, leptin and TAC levels in serum, and reduced TNF-α expression and MDA levels. The GLUT4 expression in adipose tissue was not significant between studied groups. Pioglitazone and IRAKi improved insulin function by inhibiting inflammation signaling.
    Conclusion
    According to the results of this study, IRAKi may be an appropriate target for inhibiting inflammation and related disorders, including insulin resistance.
    Keywords: Diabetes Mellitus, insulin resistance, IRAK Inhibitor, GLU4, PPARγ, Pioglitazone}
  • ابوالحسن هدایتی کتولی، محمدعلی آذربایجانی*، عبدالعلی بنائی فر، سجاد ارشدی
    زمینه و هدف

    چاقی موجب استیاتوز در کبد می شود. PPARγ فاکتور رونویسی ژن های متابولیسم گلوکز و چربی و AMPK سنسور انرژی سلول به عنوان اهداف درمانی در بیماران کبد چرب غیرالکلی (NAFLD[1]) موردتوجه می باشند. باوجود اهمیت تمرین و دارو در درمان بیماری های مزمن، در ارتباط با نقش تمرینات شدید (HIIT) در درمان NAFLD توافق کمی وجود دارد. هدف از مطالعه حاضر بررسی اثر شدت تمرین و آدنوزین بر متابولیسم چربی کبد به دنبال رژیم غذایی پرچرب بود.

    مواد و روش ها:

     30 سر موش به صورت تصادفی به 6 گروه 5تایی کنترل، غذای پرچرب، غذای پرچرب + تزریق دارونما، غذای پرچرب + تزریق آدنوزین، غذای پرچرب - تمرین + تزریق آدنوزین، غذای پرچرب - تمرین + تزریق دارونما تقسیم شدند. آزمودنی ها ابتدا 13 هفته غذای پرچرب دریافت نمودند و سپس 12 هفته، هفته ای 5 جلسه به تمرین پرداختند، در گروه های غذایی از آزمون تحلیل یک راهه واریانس مستقل و جهت تعیین اثر اصلی تمرین، آدنوزین و تمرین× آدنوزین از تحلیل دوراهه واریانس برای گروه های مستقل استفاده شد.

    نتایج

    بیان ژن PPARγ در گروه های غذایی پرچرب افزایش داشت (017/0=P)، (007/0=P). تفاوتی در بیان AMPK بین گروه های غذایی وجود نداشت (097/0=P). تمرین اثر معنی دار برافزایش بیان AMPK، A2B (0001/0=P)، (031/0=P) و کاهش معنی دار بر PPARγ (0001/0=P) داشت. در گروه آدنوزین AMPK و A2b افزایش معنی دار (001/0=P)، (012/0=P) و PPARγ کاهش داشت (0001/0=P). هم زمانی تمرین و آدنوزین افزایش معنی دارتری بر بیان AMPK (039/0=P) و کاهش معنی دارتری بر PPARγ (005/0=P) نسبت به اثر هر یک به تنهایی داشت.

    نتیجه گیری:

     احتمالا بتوان از تمرینات با شدت بالا و هم زمان مقدار مشخص دوز مصرفی آدنوزین جهت جلوگیری از تجمع چربی کبد استفاده نمود.

    کلید واژگان: تمرین تناوبی هوازی, آدنوزین, غذای پرچرب, AMPK, PPARγ, A2B, موش صحرایی}
    Abolhasan Hedayati Katooli, MohammadAli Azarbayjani*, Abdolali Banaeifar, Sajad Arshadi
    Background & Objective

    Obesity causes steatosis in the liver. PPARγ transcription factor of glucose and fat metabolism genes and AMPK cell energy sensor are considered as therapeutic targets in non-alcoholic fatty liver (NAFLD) patients. Despite the importance of exercise and medication in the treatment of chronic diseases, there is little agreement on the role of intense exercise (HIIT) in the treatment of NAFLD. The aim of this study was to investigate the effect of exercise intensity and adenosine on liver fat metabolism following a high-fat diet.

    Materials & Methods

    30 mice were randomly divided into 6 groups of 5 controls, high fat diet, high fat diet + placebo injection, high fat diet + adenosine injection, high fat diet - exercise + adenosine injection, high fat diet - exercise + placebo injection. Subjects first received 13 weeks of high-fat diet and then exercised 5 sessions per week for 12 weeks.

    Result

    PPARγ gene expression increased in high-fat food groups (P = 0.017), (P = 0.007). There was no difference in AMPK expression between food groups (P = 0.097). Exercise had a significant effect on increasing expression of AMPK, A2B (P = 0.0001), (P = 0.031) and a significant decrease on PPARγ (P = 0.0001). In adenosine group, AMPK and A2b significantly increased (P = 0.001), (P = 0.012) and PPARγ decreased (P = 0.0001). Simultaneous exercise and adenosine had a more significant increase in AMPK expression (P = 0.039) and a more significant decrease in PPARγ (P = 0.005) than the effect of each alone.

    Conclusion

    It is possible to use high-intensity exercise with a certain amount of adenosine at the same time to prevent the accumulation of fat in the liver.

    Keywords: aerobic interval training, adenosine, high-fat diet, AMPK, PPARγ, A2B, rat}
  • مریم سادات هاشمی، مریم شعبانی، سعیده شادمهری*، محمد شرافتی مقدم، محمد فتح علی پور
    سابقه و هدف

    امروزه پروتئین ها و مسیرهای سلولی مهمی شناسایی شده اند که منجر به تنظیم بافت چربی سفید و تبدیل آن به بافت چربی قهوه ای می شوند که پروتئین های PPARγ و PRDM16 پروتئین های کلیدی در این تنظیم هستند. دیابت از عوامل مهم چاقی و ایجاد عوارض می باشد که می تواند در عملکرد این دو پروتئین اختلال ایجاد کند. هدف از مطالعه حاضر، بررسی تاثیر 4 هفته تمرین تناوبی با شدت بالا (HIIT; High-Intensity Interval Training) بر محتوای پروتئین های PPARγ و PRDM16 در بافت چربی زیرجلدی موش های صحرایی نر چاق مبتلا به دیابت می باشد.

    مواد و روش ها

     در این مطالعه تجربی، 16 سر موش صحرایی نر نژاد اسپراگوداولی (با میانگین وزن 20±300 گرم) انتخاب و پس از دیابتی شدن ازطریق تزریق STZ و نیکوتین آمید به روش تصادفی به 2 گروه تمرین دیابتی و کنترل دیابتی تقسیم ‏شدند؛ گروه تمرینی 4 روز در هفته مطابق با برنامه تمرینی به‏ مدت 4 هفته به فعالیت ورزشی پرداختند؛ در حالی که گروه کنترل هیچ گونه برنامه تمرینی نداشتند. برای تجزیه و تحلیل داده ها از آزمون t-مستقل استفاده‏ شد.

    نتایج

    تغییر معنی داری در محتوای پروتئین های PPARγ (0/16=P) و PRDM16 (0/83=P) به دنبال 4 هفته تمرین HIIT در گروه تمرین نسبت به کنترل مشاهده نشد.

    نتیجه گیری

     باتوجه به نتایج تحقیق حاضر، تمرین HIIT منجر به تغییر معنی دار محتوای پروتئین های PPARγ و PRDM16 نشده است. به نظر می رسد شدت تمرین ورزشی HIIT عامل مهمی در این نتیجه باشد که باید به آن توجه کرد.

    کلید واژگان: دیابت, تمرین تناوبی با شدت بالا, PPARγ, PRDM16, بافت چربی سفید}
    Maryam Sadat Hashemi, Maryam Shabani, Saeedeh Shadmehri*, Mohammad Sherafati, Mohammad Fathalipour
    Background

    Today, important proteins and pathways have been identified that lead to the regulation of the white adipose tissue and converting it to brown adipose tissue, the proteins PPARγ and PRDM16 are key proteins in this setting. Diabetes is one of the major causes of obesity and complications that can interfere in the function of these two proteins. This study aimed to investigate the effect of 4 weeks High-Intensity Interval Training (HIIT) on the content of PPARγ and PRDM16 proteins in subcutaneous adipose tissue of diabetic obese male rats.

    Materials and Methods

    In this experimental study, 16 Sprague-Dawley male rats (mean weight of 300±20 gr) were selected and after induction of diabetes by injection of STZ and nicotinamide was randomly assigned into two groups: diabetic training and diabetic control. The experimental group performed HIIT training for 4 weeks, accordance with the training program for 4 weeks, while the control group did not have any training program. Independent T-test was used to analyze the data.

    Results

    Significant change was not observed in the content of PPARγ (P=0.16) and PRDM16 (P=0.83) proteins in HIIT training group compared to the control group.

    Conclusion

    According to the results of this study, HIIT training has not led to significant change the content of PPARγ and PRDM16 proteins. It seems to the intensity of HIIT training be a major contributor to the result that should be taken into consideration.

    Keywords: Diabetes, High-Intensity Interval Training (HIIT), PPARγ, PRDM16, White fat tissue}
  • اکبر حیدری، محمد نوری، مهزاد صدقیانی، عصمت آقاداود جلفایی*
    سابقه و هدف
    سندروم تخمدان پلی کیستیک (Polycystic ovary syndrome; PCOS) اغلب باعث کاهش اوولاسیون، ناباروری و مقاوت به انسولین می گردد. یکی از عوامل موثر در بروز این بیماری گیرنده های Proxsisome proliferative–activated receptor gamma ((PPARγ می باشند که جزو گروهی از گیرنده های هست های هستند. آگونیست های PPARγ برای درمان مقاومت به انسولین، هیپرآندروژنیسم و اختلال عملکرد تخمدان در بیماران PCOS به کار می روند. اسیدهای چرب مثل EPA (Eicosa penta enoic acid) و متابولیت های آن ها، لیگاندهای طبیعی برای PPARγ بوده و گزینه مناسبی برای تنظیم بیان این ژن محسوب می شوند.
    مواد و روش ها
    این مطالعه مورد- شاهدی روی 30 نفر از زنان مبتلا به سندروم تخمدان پلی کیستیک مراجعه کننده به مرکز باروری الزهرا تبریز جهت درمان IVF (in vitrofertilization) مراجعه کرده بودند، انجام شد. ابتدا سلول های گرانولوزا از مایع فولیکولی این افراد جمع آوری گردید و سپس در محیط آزمایشگاهی کشت داده شد. میزان بیان ژن های PPARγ و (Insulin-like growth factor 1)IGF-1 در سلول های گرانولوزا در محیط کشت و در محیط کشت به همراه EPA بررسی گردید.
    نتایج
    بیان ژن PPARγ در سلول های گرانولوزای کشت شده در محیط تیمار شده با EPA در مقایسه با محیط کشت کنترل افزایش یافت و این افزایش در غلظت 100 میکرومول و زمان 48 ساعت بیشترین مقدار بود. هم چنین، افزایش بیان PPARγ منجر به افزایش ژن های درگیر در استروئیدوژنز یعنی IGF-1 شد، درحالی که بیان هر دو ژن در بیمارانPCOS و در محیط کشت کنترل کاهش یافت.
    نتیجه گیری
    در مجموع می توان گفت کهEPA باعث افزایش بیان ژن PPARγ و به دنبال آن IGF-1 در سلول های گرانولوزای بیماران مبتلا به PCOS می شود.
    کلید واژگان: سندروم تخمدان پلی کیستیک, سلول های گرانولوزا, PPARγ, EPA}
    Akbar Heidari, Mohammad Nouri, Mahzad Sadaghiani, Esmat Aghadavod*
    Background
    Polycystic ovarian syndrome (PCOS) often induces reduced ovulation, infertility and insulin resistance. One of the most influential inducer factors in disease is peroxisome proliferator-activated receptor gamma (PPARγ) a member of the nuclear receptor superfamily, which has a variety of physiological functions. PPARγ agonists are used for the treatment of insulin resistance, hyperandrogenism and ovarian dysfunction in PCOS patients. Fatty acids like eicosapentaenoic acid (EPA) and their metabolites are natural ligands for PPARγ and a good option for regulation of PPARγ gene expression.
    Materials And Methods
    This case-control study was carried out on 30 women with PCOS referred to the Tabriz-Alzahra fertility center for in vitro fertilization (IVF). Granulosa cells collected from follicular fluid of these individuals were cultured in vitro. Gene expression of PPARγ, insulin-like growth factor 1(IGF-1) and cyclooxygenase-2 were examined on cultured granulosa cells in culture medium and EPA–mediated culture media.
    Results
    The PPARγ gene expression was increased in EPA-treated medium with a maximum expression at a concentration of 100 mmol in 48 hours. On this basis, increment of PPARγ expression lead to the increased gene expression involved in the steroidogenesis, (i.e. IGF-1). However, the exptression of both genes were decreased in PCOS and the control medium.
    Conclusion
    In this study, we observed that different concentrations of EPA increased PPARγ gene expression.
    Keywords: Polycystic ovary syndrome, IGF, 1, PPARγ, EPA}
  • Xianchu Liu, Ming Liu, Yanzhi Mo, Huan Peng, Jingbo Gong, Zhuang Li, Jiaxue Chen, Jingtao Xie*
    Objective(s)
    Previous research demonstrated that diabetes is one of the leading causes of learning and memory deficits. Naringin, a bioflavonoid isolated from grapefruits and oranges, has potent protective effects on streptozotocin (STZ)-induced diabetic rats. Recently, the effects of naringin on learning and memory performances were monitored in many animal models of cognitive impairment. However, to date, no studies have investigated the ameliorative effects of naringin on diabetes-associated cognitive decline (DACD). In this study, we investigated the effects of naringin, using a STZ-injected rat model and explored its potential mechanism.
    Materials And Methods
    Diabetic rats were treated with naringin (100 mg/kg/d) for 7 days. The learning and memory function were assessed by Morris water maze test. The oxidative stress indicators [superoxide dismutase (SOD) and malondialdehyde (MDA)] and inflammatory cytokines (TNF-a, IL-1β, and IL-6) were measured in hippocampus using corresponding commercial kits. The mRNA and protein levels of PPARγ were evaluated by real time (RT)-PCR and Western blot analysis.
    Results
    The results showed that supplementation of naringin improved learning and memory performances compared with the STZ group. Moreover, naringin supplement dramatically increased SOD levels, reduced MDA levels, and alleviated TNF-α, IL-1β, and IL-6 compared with the STZ group in the hippocampus. The pretreatment with naringin also significantly increased PPARγ expression.
    Conclusion
    Our results showed that naringin may be a promising therapeutic agent for improving cognitive decline in DACD.
    Keywords: Cognitive, DACD, Inflammation, Naringin, Oxidative stress, PPARγ}
  • حسین منتخب یگانه، حسین بابا احمدی رضایی، محمود دوستی *
    هدف

    عوامل متعددی در ایجاد بیماری های قلبی- عروقی دخیل اند، از جمله اسیدهای چرب ترانس، که به طور عمده طی فرآیندهای اشباع سازی روغن های گیاهی به وجود می آیند. این فرآیندها موجب تشکیل روغن های نیمه جامد می شود، امروزه مشخص شده است که این ماده غذایی عامل خطر مهمی در بروز و پیشرفت آتروسکلروز است؛ از طرف دیگر مشخص شده است که، تعدادی از گیرنده های هسته ای از جمله PPARها (Peroxisome Proliferator Activated Receptor) در هموستاز لیپید و پاتوژنز بیماری های قلبی- عروقی دخالت داشته و نقش های به سزایی ایفا می کنند؛ از این رو در این مطالعه تاثیر اسید الاییدیک بر بیان ژن PPARγ مورد بررسی قرار گرفته شد.

    روش بررسی

    سلول های ماکروفاژی RAW264.7 با غلظت های mM5/0، یک و دو اسید الاییدیک به مدت شش ساعت تیمار گردیدند. گروه کنترل نیز حاوی اتانول 50% (به عنوان حلال) معادل مقدار اتانول استفاده شده در غلظت دو میلی مولار لحاظ گردید. بعد از استخراج RNA و سنتز cDNA میزان بیان ژن PPARγ با روش Real-Time PCR مورد سنجش قرار گرفت.

    یافته ها

    اسید الاییدیک بعد از تیمار شش ساعته در هر سه غلظت mM5/0، یک و دو میزان بیان ژن PPARγ را در رده سلولی ماکروفاژی RAW264.7 در مقایسه با گروه کنترل، به ترتیب 36/1، 68/1 و 24/3 برابر کاهش داد (05/0P<).

    نتیجه گیری

    اسید الاییدیک، از طریق کاهش بیان ژن گیرنده هسته ای PPARγ باعث بروز، تشدید و یا تسریع بیماری های قلبی و عروقی به خصوص آتروسکلروز می شود و این یافته اهمیت کاهش مصرف این ماده غذایی را نشان می دهد.

    کلید واژگان: کشت سلول, اسید الاییدیک, آتروسکلروز, بیان ژن, اسید چرب ترانس, PPARγ}
    Hossein Montakhab Yegane, Hossein Babaahmadi Rezaiy, Mahmood Doosti
    Background

    Several dietary factors are involved in cardiovascular coronary heart diseases, including trans fatty acids, which are generally formed during hydrogenation of vegetable oils, a process that causes conversion of liquid oils into semisolid fats. Nowadays, it is well-known that trans fatty acids form a major risk factor in the occurrence and progression of atherosclerosis. On the other hand, it has been identified that some nuclear receptors, such as PPARs, are involved and play important roles in lipid homeostasis and pathogenesis of cardiovascular diseases. Therefore, we studied the effect of elaidic acid on gene expression of peroxisome proliferator activated receptor gamma (PPARγ).

    Methods

    Murine macrophage RAW264.7 cells were treated by 0.5, 1, and 2 mM concentrations of elaidic acid for 6 h. The control group was treated by 50% ethanol (as solvent), equivalent to the amount of ethanol used in 2 mM concentration of elaidic acid. Later, the total RNA was extracted and its cDNA was synthesized. Finally, the quantity of PPARγ gene expression was measured by real-time PCR.

    Results

    Overall, 0.5, 1, and 2 mM concentrations of elaidic acid decreased PPARγ gene expression in RAW264.7 macrophage cell line by -1.36, -1.68, and -3.24 folds compared with the control group, respectively.

    Conclusion

    By decreasing the expression of nuclear receptor PPARγ, elaidic acid causes, intensifies or accelerates the occurrence of cardiovascular diseases, especially atherosclerosis. This finding shows the importance of reducing the consumption of elaidic acid containing foods.

    Keywords: atherosclerosis, cell culture, elaidic acid, gene expression, trans fatty acids, PPARγ}
نکته
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