جستجوی مقالات مرتبط با کلیدواژه "pro-inflammatory cytokines" در نشریات گروه "پزشکی"
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BackgroundThe efficacy of low-dose rate ionizing radiation (LDRIR) for anti-inflammatory treatment has been confirmed in various clinical studies. However, the radiobiological mechanisms involved in the anti-inflammatory action of LDRIR have not been completely elucidated.Materials and MethodsThis study investigated whether LDRIR at 0.5 or 1 Gy affected the regulation of cytokine messenger RNA expression and protein levels in inflamed synoviocytes and chondrocytes induced by lipopolysaccharide. Intercellular adhesion molecule-1, interleukin-6, interleukin-8, and growth-regulated alpha protein expression were analyzed in synoviocytes and chondrocytes at 24 h after lipopolysaccharide treatment using reverse transcription polymerase chain reaction, immunostaining, Western blotting, and enzyme-linked immunosorbent assays.ResultsThe messenger RNA expression levels of interleukin-6, interleukin-8, and growth-regulated alpha protein were lower in synoviocytes cotreated with lipopolysaccharide and 0.5 or 1 Gy radiation than in those treated with lipopolysaccharide alone. The immunostaining results showed that all target cytokines were downregulated after 0.5 and 1 Gy of radiation in inflamed synoviocytes and chondrocytes. In chondrocytes, all four cytokines were significantly downregulated at a dose rate of 0.053 Gy/min, and the extent of regulation was similar to that at 4.02 Gy/min.ConclusionOur findings indicate that LDRIR may regulate pro-inflammatory cytokine expression in both synoviocytes and chondrocytes, regardless of the dose rate. Therefore, LDRIR can alleviate concerns of carcinogenesis and may be useful in clinical settings.Keywords: Low-Dose Radiotherapy, Anti-Inflammation, Synoviocytes, Chondrocytes, Pro-Inflammatory Cytokines
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مقدمه
تحت شرایط هیپرگلیسمی، فرآیندهای التهابی با آسیب به اعصاب محیطی در بروز نوروپاتی دخیل هستند. این مطالعه با هدف بررسی مقایسه ای اثرات ضد التهابی متفورمین (داروی سنتزی) با گالیک اسید (ترکیب طبیعی) در شرایط هیپرگلیسمی صورت گرفت.
روش هابرای القای هیپرگلیسمی به موش های صحرایی، استرپتوزوتوسین (STZ) با دوز mg/kg 60 به صورت داخل صفاقی تزریق شد. برای این تحقیق موش ها در چهار گروه قرار گرفتند. دو گروه موش های کنترل سالم و هیپرگلیسمی بودند که دارویی دریافت نکردند. دو گروه دیگر، موش های هیپرگلیسمی بودند که به ترتیب، متفورمین با دوز mg/kg/day 300 و گالیک اسید با دوز mg/kg/day 40 دریافت نمودند. در پایان دوره 8 هفته ای، موش ها را در تمام گروه ها بیهوش کرده و نمونه ای از عصب سیاتیک برای سنجش میزان بیان ژن های مربوط به سیتوکین های پیش التهابی IL-6، IL-1β و TNF-α، گرفته شد. آنالیز داده ها توسط نرم افزار SPSS و مقایسه بین میانگین داده ها توسط آنالیز واریانس یک طرفه (one-way ANOVA) و آزمون تعقیبی Tukey صورت گرفت.
یافته هاالقای شرایط هیپرگلیسمی به موش های صحرایی باعث افزایش بیان ژن های مربوط به سیتوکین های پیش التهابی IL-6 (000/0 =P)، IL-1β (008/0 =P) و TNF-α (005/0 =P) شد، اما تجویز متفورمین و گالیک اسید به موش های صحرایی هیپرگلیسمی به مدت 8، میزان بیان ژن های IL-6، IL-1β و TNF-α را کاهش داد (05/0 ˂p).
نتیجه گیریگالیک اسید همانند متفورمین، با ویژگی ضد التهابی خود، می تواند برای بهبود عوارض ناشی از شرایط هیپرگلیسمی به ویژه التهاب عصبی موثر واقع شود و امید است در آینده برای بیماران دیابتی کاربرد بالینی داشته باشد.
کلید واژگان: ضد التهابی, گالیک اسید, هیپرگلیسمی, متفورمین, سیتوکین های پیش التهابیBackgroundUnder hyperglycemic conditions, inflammatory processes with damage to the peripheral nerves are involved in the occurrence of neuropathy. This study aimed to compare the anti-inflammatory effects of metformin (synthetic drug) with gallic acid (natural compound) in hyperglycemic conditions.
MethodsHyperglycemia was induced in male rats by the intraperitoneal injection of Streptozotocin (STZ) at a dose of 60 mg/Kg. For this research, rats were divided into four groups. Two groups were healthy control and hyperglycemic control rats that did not receive any drugs. The other two groups were hyperglycemic rats, which respectively received Metformin at a dose of 300 mg/kg/day and gallic acid at a dose of 40 mg/kg/day. At the end of the 8-week period, the rats in all groups were anesthetized and a sample of their sciatic nerve was taken to measure the expression level of genes related to pro-inflammatory cytokines IL-6, IL-1β and TNF-α. Data analysis was done by SPSS software and comparison between average data was done by one-way ANOVA and Tukey's post hoc test.
ResultsInduction of hyperglycemic conditions in rats increased the expression of genes related to pro-inflammatory cytokines IL-6 (p=0/000), IL-1β (p=0/008) and TNF-α (p=0/005). However, administration of metformin and gallic acid to hyperglycemic rats for 8 weeks reduced the expression of IL-6, IL-1β and TNF-α genes (p˂0.05).
ConclusionGallic acid, like metformin, with its anti-inflammatory properties, can be effective in improving complications caused by hyperglycemic conditions, especially neuroinflammation, and it is hoped that it will be clinically useful for diabetic patients in the future.
Keywords: Anti-Inflammatory, Gallic Acid, Hyperglycemia, Metformin, Pro-Inflammatory Cytokines -
Background and Aim
To investigate the association of adipose tissue transcript levels of IL-1β, IL-6, TNF-α, and MCP-1 with various adiposity indices in obese women.
MethodsReal-time PCR was carry out to investigate the mRNA expression level of the mentioned genes in VAT and SAT from all participants.
ResultsThe results presented higher mRNA levels of IL-6 and MCP-1 in SAT and VAT of obese women, compared to normal-weight women. As well, results showed a positive correlation of IL-6 and MCP-1 with HOMA-IR. Obesity indices including BMI, hip, and WHtR were considerably higher in the obese group in comparison with the control group. More importantly, we observed a positive correlation of mRNA expression of these pro-inflammatory factors in adipose tissues with some obesity indices.
ConclusionWe have shown here that adipose tissue transcript levels of pro-inflammatory cytokines were significantly higher in obese participate than non-obese participants. In obese individuals, this proinflammatory molecules was significantly correlated with various obesity indices. These results suggest that targeting obesity and adipose tissue could prevent the high expression of cytokine.
Keywords: Adipose Tissue, Pro-inflammatory Cytokines, Adiposity Indices, Anthropometric Index, Obesity -
Background
Gastrointestinal (GI) mucositis is one of the serious side effects of methotrexate (MTX) treatment. It is known that oxidative stress plays an important role in drug-induced side effects.
ObjectivesThe present study aimed to assess the effect of gallic acid (GA) against MTX-induced intestinal mucositis in male Wistar rats.
MethodsTwenty-eight adult male Wistar rats were randomly divided into 4 groups (n = 7), including (1) control group; (2) GA group (gallic acid: 30 mg/kg/day, orally); (3) MTX group [20 mg/kg, intra peritoneal (IP)]; and (4) (MTX + GA) group (MTX: 20 mg/kg, IP and gallic acid: 30 mg/kg/day, orally). Then amounts of malondialdehyde (MDA), nitric oxide (NO), glutathione peroxidase (GPx), glutathione (GSH), superoxide dismutase (SOD), interleukin 2 (IL-2) and interleukin 6 (IL-6) were analyzed in serum samples and then the histopathological examinations of the duodenum and jejunum of animals groups.
ResultsThe results showed that treatment with GA significantly reduced the MTX-induced elevation of serumMDA(P < 0.001), NO (P < 0.001), IL-2 (P < 0.001) and IL-6 (P < 0.001) contents and increased MTX-induced reduction in GSH (P < 0.001) content, GPx (P < 0.001) and SOD (P < 0.001) activity. In addition, the histopathological results showed that MTX leads to intestinal tissue damage, and gallic acid can remarkably improve the pathological changes.
ConclusionsOur results indicate that gallic acid can mitigate oxidative stress and pro-inflammatory parameters and also moderately prevent histopathological damage of the small intestine of rats exposed to MTX.
Keywords: Methotrexate, Intestinal Mucositis, Gallic Acid, Oxidative Stress, Pro-inflammatory Cytokines, Histopathology -
بررسی اثرات ضد دردی، ضد التهابی و آنتی اکسیدانی جنیستئین و ورزش شنا در موش های صحرایی اواریکتومی شدهزمینه و هدف
یایسگی و مخصوصا یایسگی حاد در اثر جراحی با مشکلات متعددی در زنان همراه میباشد. هدف این مطالعه تعیین اثرات جنیستیین و ورزش منظم شنا (به تنهایی/ یا ترکیبی) بر درد از طریق مکانیسم احتمالی التهابی و استرساکسیداتیو در موشهای صحرایی اواریکتومی شده بود.
روش کاردر این مطالعه موشهای صحرایی به شش گروه شامل: گروه کنترل، گروه شم، گروه اواریکتومی شده (OVX)، گروه اواریکتومی شده با هشت هفته تمرین ورزشی شنا (OVX.E)، گروه اواریکتومی شده با هشت هفته تجویز جنیستیین (OVX.G) و گروه اواریکتومی شده با هشت هفته درمان ترکیبی ورزش و جنیستیین (OVX.G.E) تقسیم شدند. اثرات جنیستیین و/ یا ورزش با بررسی شدت درد با استفاده از تستهای تیل- فلیک و فرمالین ارزیابی شد. سطوح سرمی اینترلوکین یک بتا (IL-1β) و فاکتور نکروز توموری آلفا (TNF-α) و سطح ظرفیت آنتیاکسیدانی کل (TAC)، وضعیت اکسیدان کل (TOS) و مالون دیآلدیید (MDA) توسط ELISA و اسپکتروفتومتر ارزیابی شدند.
یافته هادر گروه OVX در مقایسه با گروه کنترل، آزمایشات تیل- فلیک و فرمالین نشان از افزایش پاسخ درد داشتند. همچنین افزایش معنیداری در سطوح سرمی فاکتورهای IL-1β، TNF-α، MDA، TOS و کاهش TAC، در گروه OVX مشاهده شد؛ ولی در گروههای OVX.E، OVX.G و مخصوصا OVX.E.G سایتوکینهای پیش التهابی و استرس اکسیداتیو و همچنین پاسخهای درد کاهش معنی داری نسبت به گروه OVX از خود نشان دادند.
نتیجهگیری:
ترکیبی از جنیستیین و ورزش منظم شنا دارای اثر همافزایی و محافظتی بیشتری در کاهش درد حاد و مزمن نسبت به استفاده از این روشها به تنهایی در دوره یایسگی است.
کلید واژگان: درد پس از یائسگی, جنیستئین, ورزش, سایتوکین های التهابی, استرس اکسیداتیوBackground & objectivesMenopause and especially acute menopause due to surgery is associated with many complications in women. The aim of this study was to determine the effects of genistein and regular swimming exercise (alone/or in combination) on pain through a possible mechanism of inflammation and oxidative stress in ovariectomized rats.
MethodsIn this study, rats were divided into six groups, including: control, sham, ovariectomy (OVX), ovariectomized with eight weeks of swimming exercise training (OVX.E), ovariectomized with eight weeks of genistein administration (OVX.G), and ovariectomized with eight weeks of combined treatment (OVX.G.E). The effects of genistein and/or exercise were evaluated by examining the pain intensity with tail-flick and formalin tests. The serum levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), total antioxidant capacity (TAC), total oxidant status (TOS), and malondialdehyde (MDA) were also evaluated by ELISA and spectrophotometer.
ResultsIn the OVX group compared to the control group, tail-flick and formalin tests showed an increase in pain response. Also, a significant increase in the serum levels of IL-1β, TNF-α, MDA, TOS and a decrease in TAC was observed in the OVX group, however, in the OVX.E, OVX.G and especially OVX.E.G groups, pro-inflammatory cytokines and oxidative stress as well as pain responses showed a significant decrease compared to the OVX group.
ConclusionA combination of genistein and regular swimming exercise was synergistically more effective in reducing acute and chronic pain than using them alone in the postmenopausal period.
Keywords: Postmenopausal Pain, Genistein, Exercise, Pro-inflammatory Cytokines, Oxidative Stress -
زمینه و هدف
هنوز تاثیر تمرین شنا بر سطوح سایتوکاین های پیش التهابی و التهابی نظیر اینترلوکین-6 و اینترلوکین-10 و در نتیجه بر میزان حافظه فضایی در رت های بالغ به طور دقیق مطالعه نشده است؛ لذا هدف این مطالعه تعیین اثر تمرین شنا بر حافظه فضایی و سطوح التهاب هیپوکامپ در موش ها بود.
روش کارموش های نر نژاد C57BL6 با (سن تقریبی 10-11هفته) و (وزن 18-21 گرم) از انستیتو پاستور ایران تهیه و در شرایط نوری 12 ساعت روشنایی و 12 ساعت تاریکی و دمای 23±1 درجه سانتیگراد و رطوبت 40-50 درصد نگهداری و آب و غذای کافی به صورت آزاد در دسترس آن ها قرار داده شد. حیوانات به دو گروه بدون تمرین و با تمرین شنا (8 سر در هرگروه) تقسیم شدند؛ سپس حیوانات تحت یک برنامه 4 هفته ای تمرین شنا قرار گرفتند. داده ها با استفاده از آنالیز تی تست مورد بررسی قرار گرفت.
یافته هاموش هایی که ورزش شنا تجربه کرده اند سطح بالاتری از سایتوکاین اینترلوکین 10 را در هیپوکامپ خود نسب به گروه کنترل نشان داده اند و اثر معناداری تمرین شنا بر حافظه فضایی تایید شد. همچنین ورزش شنا منجر به کاهش سطح التهاب هیپوکامپ از طریق کاهش سطح اینترلوکین-6 در مقایسه با موش های گروه کنترل شد.
نتیجه گیریدر مجموع، این مطالعه نشان می دهد که ورزش شنا ممکن است بتواند به عنوان یک استراتژی غیردارویی مکملی برای درمان زوال شناختی در افراد مبتلا پیشنهاد گردد. با این وجود، مطالعات بیشتر باید بر پروتکل های آموزشی که می تواند در انسان استفاده شود، متمرکز شود.
کلید واژگان: تمرین شنا, سایتوکاین های پیش التهابی, سایتوکاین های التهابیBackground & AimsThe lifestyle in the machine world of the last century is low mobility and very little activity with the use of various types of equipment and facilities. This lifestyle is the basis of many physical and mental complications in today's humans and causes the occurrence of many chronic diseases such as diabetes and obesity, increased blood pressure, and metabolic syndrome as a whole, followed by widespread inflammation in the body. Increased inflammation in the body, especially in the central nervous system of the brain, can lead to neurological and behavioral disorders. The immune system plays an important role in regulating brain homeostasis. Even small amounts of Neuroinflammation can disrupt physiological processes that occur in the hippocampus, including neurogenesis. Inflammatory factors include inflammatory cytokines such as interleukin 6 and alpha necrosis factor. In recent years, human and animal studies have shown that the increase of these two cytokines in the body and brain can lead to a decrease in memory. However, its exact mechanisms are not fully understood. Recent findings also show that IL-6 is involved in cognitive functions and memory, and increasing its level in brain areas such as the hippocampus may lead to a decrease in memory, on the other hand, anti-inflammatory factors such as IL-10 (potential role in immunotherapy and prevention) And progress or recurrence of neuropathy play a role in the body. Interleukin 10 prevents the production and secretion of inflammatory cytokines. This cytokine is secreted to suppress pro-inflammatory effects in stressful situations. The most important brain region involved in cognitive functions and memory is the hippocampus. Any damage to nerve cells in this area of the brain can be directly related to cognitive disorders. Exercise is known as a risk modulating factor for reducing memory and learning in neurological diseases and even Alzheimer's disease. It is assumed that neurological and vascular adaptation to exercise and physical activity improves cognitive function through neurogenesis, reducing pro-inflammatory processes and reducing cell damage. Physical activity can modulate microglial activation in the CNS. Low-intensity exercise is sufficient to induce an anti-microglial activation effect by regulating the expression of various factors. Some of these factors (eg, Myokines) can directly prevent microglial activation through various mechanisms that prevent Neuroinflammation in the CNS. Be secreted from different sources (such as damaged neurons, astrocytes, and microglia). According to past research and since the effect of swimming exercise on the amount of pro-inflammatory and inflammatory cytokines such as IL-6 and IL-10 and as a result on the amount of spatial memory in adult rats has not been investigated, this research was conducted in order to make its results for patients suffering from memory loss. It should be implemented in clinics as a suggested non-pharmacological and effective treatment, especially in elderly people who have been diagnosed with Alzheimer's disease.
MethodsC57BL6 male mice (approximate age 10-11 weeks) and (weight 18-21 grams) were obtained from Pasteur Institute of Iran and kept under light conditions of 12 hours of light and 12 hours of darkness (8 am to 8 pm) and a temperature of 1±23 degrees Celsius and humidity of 40-50% and enough water and food were freely available to them. The data were analyzed using t-test analysis and P<0.05 was considered significant. SPSS software was used for analysis and GraphPad Prism software (V8.5) was used for drawing graphs.
ResultsMice who have experienced swimming showed a higher level of the cytokine interleukin 10 in their hippocampus compared to the control group (p=0.002) and the significant effect of swimming training on spatial memory was confirmed and swimming led to a decrease in hippocampal inflammation. Through the reduction of interleukin 6 levels compared to control group mice (p=0.025).
ConclusionIn this study, the effect of swimming training on the amount of inflammatory and anti-inflammatory factors and spatial memory was investigated, and according to the tests and results obtained, it was determined that swimming training has a significant effect on the reduction of the inflammatory factor interleukin-6 and the increase of the anti-inflammatory factor interleukin-10. It is effective in reducing the number of cognitive disorders, including spatial memory. Aerobic exercise can partially reverse the cognitive decline associated with diabetes by reducing the oxidative stress and inflammatory environment in the brain of T2D animals. Regular exercise has significant benefits on insulin sensitivity in adults with type 2 diabetes and may persist for more than 72 hours after the last exercise session. Long-term intense exercise can generally lead to higher levels of inflammatory mediators and thus may increase the risk of injury and chronic inflammation. In contrast, moderate exercise or vigorous exercise with adequate rest periods can achieve maximum benefit. Exercise can protect against age-related cognitive decline, Alzheimer's disease (AD), and vascular dementia. We provide evidence of swimming exercise in other animal models that assess cognitive functions and hippocampal inflammatory and Neurotrophic systems. In support of our data, studies are showing that swimming exercise can improve cognitive deficits in various animal models. Regular swimming exercise in mice significantly increases working, spatial and cognitive memory in Alzheimer's disease conditions or is effective in healthy conditions as well. Overall, this study shows that swimming exercise may be suggested as a complementary non-pharmacological strategy for the treatment of cognitive decline in affected individuals. However, further studies should focus on training protocols that can be used in humans.
Keywords: Swimming Exercise, Pro-Inflammatory Cytokines, Inflammatory Cytokines -
Objective(s)Ischemia-reperfusion injury is a life-threatening clinical problem that can occur after transplantation or a number of clinical procedures. The purpose of the study was to investigate the effects of Ambroxol on kidney damage caused by experimentally induced ischemia-reperfusion injury in rats.Materials and MethodsWistar albino rats were divided into 3 groups: Control (CTR, n=6), Kidney ischemia-reperfusion (K-IR, n=6), And kidney ischemia reperfusion+Ambroxol (K-IR+AMB, n=6). In K-IR+AMB group, Ambroxol (30 mg/kg) was administered orally 30 min before the ischemia period. K-IR and K-IR+AMB groups underwent 45 min of kidney ischemia followed by a 6-hour reperfusion period. At the end of the reperfusion period, blood and kidney tissue samples were collected after euthanasia. From the blood samples, BUN and creatinine levels were determined to assess kidney function, and TNF-α and IL-1β concentrations were evaluated to determine inflammatory response.ResultsWhile serum BUN, creatinine activities, and TNF-α and IL-1β concentrations were higher in both IR groups compared with the CTR group, these values were found to be lower in the K-IR+AMB group compared with the K-IR group. Histopathological examination revealed that interstitial edema and desquamation of tubular cells in the K-IR group were more severe than in the K-IR+AMB group.ConclusionAmbroxol treatment alleviated the production of pro-inflammatory cytokines and the harmful cellular effects in the tubular cells.Keywords: Ambroxol, Distant organ effect, Kidney ischemia reperfusion, Pro-inflammatory cytokines, Rat
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Background
It is believed that activation of microglia in the central nervous system upon detection of stimulus like lipopolysaccharides provokes neuroinflammation via the production of pro-inflammatory mediators and cytokines. The cytoprotective and anti-inflammatory properties of various folk medicine has been gaining attention as a strategy to combat various disease. This study aimed to assess the antineuroinflammatory properties of chloroform extract of in vitro Panax ginseng root culture based on nitric oxide and cytokines production.
MethodsThe study was initiated with the determination of maximum non-toxic dose (MNTD) of P.ginseng root culture chloroform extract using the MTT assay. The lipopolysaccharides-stimulated BV2 microglia cells were treated with MNTD and ½MNTD of the extract and its anti-neuroinflammatory properties were assessed by measuring the production of nitric oxide (NO) via Griess assay, as well as TNF-α, IL-6 and IL-10 using Quantikine ELISA.
ResultsIt was found that the MNTD and ½MNTD of the extract did not play a significant role in the production of pro-inflammatory cytokines such as NO, TNF-α and IL-6. However, the MNTD and ½MNTD of chloroform extract significantly increased the anti-inflammatory IL-10 compared to the untreated cells.
ConclusionsWith this, the chloroform extract of P. ginseng root culture potentially exerts antineuroinflammatory properties.
Keywords: Anti-inflammatory cytokines, Ginsenosides, Microglia cells, Neuroinflammation, Pro-inflammatory cytokines -
BACKGROUND
Parkinson’s disease is a neurodegenerative disorder characterized by degeneration of dopaminergic neurons in the substantia nigari. Previous studies have shown that Helicobacter pylori (H. pylori) infection is associated with treatment and clinical response to Parkinson’s disease. In the present study, we aimed to investigate the effect of H. pylori infection in the pathogenesis of Parkinson’s disease.
METHODS75 patients who suffered from Parkinson’s disease and H. pylori infection and 91 healthy controls were recruited. All the subjects were evaluated for serum IgM, IgG, and IgA antibodies as well as TNF-α, IL-6, and IL-4 cytokines by Enzyme-Linked ImmunoSorbent Assay (ELISA)methods.
RESULTSThe participants included 102 men and 64 women with a mean age of 66±10.2 and 52.6±10.7 years in the patients and control groups, respectively. The level of IgG, TNF-α, IL-6 in the patients with Parkinson’s infected with H. pylori was significantly more than that in the control group. In contrast, IgA was significantly lower in patients with Parkinson’s disease compared with the control group.
CONCLUSIONProbably, persistent infection with H. pylori could be effective in the pathogenesis of Parkinson’s disease by dominating the systemic inflammatory profile. It is suggested that pro-inflammatory cytokines followed by H. pylori infection through the promotion of immune response or neurotoxicity might have a role in the pathogenesis of Parkinson’s disease.
Keywords: Parkinson’s disease, Helicobacter pylori, Pro-inflammatory cytokines, Anti H. pyloriantibodies -
Introduction
Antidesma thwaitesianum Müll. Arg is a tropical fruit, which has been commonly used for healthy food and traditional herbal medicine. This study aimed to investigate the anti-inflammatory effects of A. thwaitesianum fruit extract (AFE) rich in 5-hydroxymethylfurfural (5-HMF) in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages.
MethodsThe chemical composition of AFE was analysed by gas chromatography/mass spectrometry (GC/MS). RAW264.7 cells were used as an in vitro inflammatory response model. RAW264.7 cells were pre-treated with various concentrations of AFE or 5-HMF and subsequently treated with LPS. Cell viability was assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The production levels of pro-inflammatory cytokines and mediators, including nitric oxide (NO), interleukin (IL)-1β, and tumour necrosis factor (TNF)-α were determined by the Griess assay and enzyme-linked immunosorbent assay. The protein expression of inducible nitric oxide synthase (iNOS) was examined by western blot analysis.
ResultsAFE had a high content of 5-HMF (61.03% ± 0.49%). Pre-treatment with AFE and 5-HMF markedly reduced LPS-induced pro-inflammatory mediators and cytokines, namely NO, IL-1β, and TNF-α, in RAW264.7 cells; this reduction correlated with downregulation of iNOS expression.
ConclusionThis study suggests that A. thwaitesianum fruit extract containing 5-HMF could modulate the LPS-induced inflammatory response by inhibiting NO, IL-1β, and TNF-α production and iNOS expression. A. thwaitesianum fruit extract rich in 5-HMF could be considered a potential therapeutic agent for the prevention of inflammation.
Keywords: Inflammation, Nitric oxide, Pro-inflammatory cytokines, Inducible nitric oxide synthetase, Tumour necrosis factor, Interleukin -
Background and purpose
Inflammatory bowel disease (IBD) is a chronic gastrointestinal disease characterized by the inflammation of the intestine. The available medicinal treatments for IBD are not efficacious enough since they exert various adverse effects. Therefore, the search for new therapeutic agents should be continued. The present study aimed to assess the anti-inflammatory effects of pregabalin on acetic acid-induced colitis in rats.
Experimental approachUsing 2 mL of 3% acetic acid solution, colitis was intra-rectally induced in rats. Animals were randomly divided into 6 groups including the normal group, colitis control group, pregabalin treatment groups (30, 50, and 100 mg/kg; i.p., respectively), and dexamethasone treatment group (1 mg/kg; i.p.). Macroscopic, microscopic, and biochemical (myeloperoxidase, tumor necrosis factor-alpha, interleukin-6, and interleukin-1 beta) examinations were used to evaluate the efficacy of pregabalin in the inflamed colon.
Findings/ ResultsAll the applied doses of pregabalin significantly decreased the severity of macroscopic and microscopic colonic damages including ulcer severity, ulcer area, percentage of necrosis, and total colitis index compared to the colitis control group. These results were confirmed by the reduced colonic concentration of tumor necrosis factor-alpha, interleukin-6, interleukin-1 beta, and myeloperoxidase activity.
Conclusion and implicationsResults of this study indicated that pregabalin administration has beneficial effects upon the treatment of experimental colitis, which might be partly due to its anti-inflammatory properties.
Keywords: Experimental colitis, Pregabalin, Pro-inflammatory cytokines, Rat -
Objective
Research suggests that fine particulate matter (PM2.5) contributes to the expansion and development of atherosclerosis. Infiltration and proliferation of vascular smooth muscle cells (VSMCs) from the blood vessel media into the intima, is an important step in the atherosclerosis pathophysiology. Afrocyclamin A, is an oleanane-type triterpene saponin, isolated from Androsace umbellate, which is commonly used in Chinese herbal medicine. In the study, we examined the effect of Afrocyclamin A on PM2.5-induced VSMCs proliferation and scrutinized possible mechanisms of action.
Materials and MethodsIn the experimental study, counting Kit-8 (CCK-8) assay was used for estimation of VSMCs viability. BrdU immunofluorescence was used for estimation of VSMCs proliferation. The levels of antioxidant parameters such as malonaldehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH); proinflammatory cytokines such as interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), nitric oxide (NO), endothelin-1 (ET-1), and vascular cell adhesion molecule-1 (VCAM-1), were estimated. The expression of proliferating cell nuclear antigen (PCNA) and phospho-p38 MAPK (p-p38 MAPK) was assessed.
ResultsCompared to PM2.5-treated cells, in addition to reducing PM2.5-induced VSMCs proliferation, Afrocyclamin A reduced the expression of PCNA and p-p38 MAPK, down-regulated the level of TNF-α, IL-1β, IL-6, VCAM-1, MDA and ET-1, and up-regulated SOD, GSH and NO level. Furthermore, the anti-proliferative effect of Afrocyclamin A was considerably increased following co-incubation of Afrocyclamin A with SB203580 (p38 MAPK inhibitor) in comparison with Afrocyclamin A-treated cells.
ConclusionBased on the results, we can conclude that Afrocyclamin A might reduce PM2.5-induced VSMCs proliferation via reduction of p38 MAPK signaling pathway
Keywords: Afrocyclamin A, Cardioprotective, Pro-Inflammatory Cytokines, p38 Mitogen-Activated Protein Kinase -
پیش زمینه و هدف
تحقیقات اخیر نقش مهم لنفوسیت های Th17 و سایر سایتوکاین ها را در پاتوژنز بیماری اسکلروز متعدد مشخص نموده اند. باوجودی که مطالعات قبلی موید نقش ضدالتهابی تروگزروتین بودند، ولی تاکنون اثرات تروگزروتین بر روی بیماری اسکلروز متعدد موردمطالعه قرار نگرفته است. در این مطالعه اثرات درمانی تروگزروتین بر روند آنسفالومیلیت تجربی خودایمن، از طریق کاهش تولید سایتوکاین های پیش التهابی IL-17، IL-1 TNF-α و کاهش سطح نیتریک اکساید و کاهش تکثیر سلول های ایمنی، مورد ارزیابی قرار گرفت.
مواد و روش کاربیماری آنسفالومیلیت تجربی خودایمن با استفاده از پپتید MOG35-55 و ادجوانت کامل فروند در موش های ماده ی C57BL/6 ا لقا شد. سپس موش ها در چهار گروه 5 راسی قرار گرفتند. در گروه درمانی بعد از ظهور علایم بالینی بیماری، درمان با تروگزروتین (روزانه 135 میلی گرم به ازای کیلوگرم وزن بدن) آغاز شد. تا زمان کشتار موش ها در روز بیست و یکم علایم بیماری به صورت روزانه ثبت گردید. سپس میزان تکثیر سلول های ایمنی به وسیله ی آزمون MTT، میزان تولید سایتوکاین ها به وسیله ی ELISA و میزان تولید نیتریک اکساید توسط آزمون گریس سنجیده شد.
یافته هاتروگزروتین پس از بروز علایم به طور معنی داری موجب تخفیف بیماری گشت. تروگزروتین موجب کاهش معنی دار تولید سایتوکاین های پیش التهابی IL-17، IL-1 TNF-α و کاهش سطح نیتریک اکساید، هم زمان با کاهش تکثیر سلول های ایمنی شد (P<0.05).
بحث و نتیجه گیریدرمان با تروگزروتین پس از بروز علایم آنسفالومیلیت تجربی خودایمن ضمن کاهش تکثیر سلول های ایمنی خود واکنش گر و کاهش در سطح سایتوکاین های پیش التهابی و نیتریک اکساید، موجب بهبود بیماری می گردد.
کلید واژگان: آنسفالومیلیت تجربی خودایمن, تروگزروتین, سایتوکاین پیش التهابی, سلول های ایمنیBackground & AimsRecent studies have demonstrated an important role for Th-17 lymphocytes and other cytokines in pathogenesis of multiple sclerosis. Although previous studies have demonstrated the anti-inflammatory potential of troxerutin, the effects of troxerutin on multiple sclerosis have not been studied so far. The present study was carried out to investigate the therapeutic effects of troxerutin on experimental autoimmune encephalomyelitis (EAE) by reducing the production of pro-inflammatory cytokines IL-17, IL-1, TNF-α, and reducing nitric oxide levels and reducing immune cell proliferation.
Materials & MethodsEAE was induced by MOG35-55 peptide and complete Freundchr('39')s adjuvant in female C57BL/6 mice. The mice were placed in four therapeutic groups of 5. Treatment with troxerutin (135 mg/kg daily) was started in the treatment group when they developed a disability score. Signs of disease were recorded daily until the day 21 when mice were sacrificed. Then, Immune cells were tested to assess proliferation rate, cytokine, and nitric oxide by the 3-(4,5 dimethylthiozol-2-yl)-2,5- diphenyl-tetrazolium bromide (MTT) assay, enzyme-linked immunosorbent assay (ELISA), and Greiss, respectively.
ResultsThe troxerutin significantly decreased the clinical signs of established EAE. Troxerutin significantly decreased the production of pro-inflammatory cytokines IL-17, IL-1 TNF-α and decreased levels of nitric oxide, while reduced the proliferation of immune cells (p<0.05).
ConclusionParallel with decreasing proliferation of Immune cells and cytokine production, troxerutin ameliorated established EAE.
Keywords: Experimental autoimmune encephalomyelitis, pro-inflammatory cytokines, troxerutin, Immune cells -
مجله دانشگاه علوم پزشکی شهید صدوقی یزد، سال بیست و هشتم شماره 5 (پیاپی 165، امرداد 1399)، صص 2614 -2634مقدمه
جراحات متنوعی سبب ایجاد یک پاسخ التهابی در بدن میزبان می شوند. از جمله این جراحات می توان به استرس جراحی اشاره کرد. جراحی، استرسی را بر بدن اعمال می کند سندرم التهابی سیستمیک انعکاسی از درجه استرس جراحی است و به عنوان یک سیستم ارزیابی کننده شدت استرس پس از جراحی را نشان می دهد. کمپلکس منظمی از مولکول های پلی پپتیدی التهابی در بروز این پاسخ التهابی مشارکت می کنند که به عنوان سایتوکین شناخته می شوند. عدم کنترل موضعی در آزاد شدن این سایتوکین ها، سبب بروز التهاب سیستمیک می شود و به طور بالقوه عوارض ویرانگری را پی دارد.در نگارش این مقاله مروری از مقالات نمایه شده در پایگاه های اطلاعاتیScience Direct, Scopus, Pubmed Springer Science و Google scholar استفاده شدند. مجموعه مقالات بررسی شده شامل 92 مقاله بود که تحقیقات کیفی و کمی مربوط به 40 سال (از سال 1979 تا سال 2019) را به زبان انگلیسی دربرداشت. این مقاله مروری بر پایه 92 مقاله مذکور و با استفاده از کلمات کلیدی استرس جراحی، سندرم پاسخ التهابی سیستمیک، سایتوکین های پیش برنده التهابی، سایتوکین های ضد التهابی نگارش شده است.مطالعات انجام گرفته روی انسان و مدل های حیوانی، پیشنهاد می کنند که هر دو نوع سایتوکین های پیش برنده التهابی و ضد التهابی متعاقب تحریکات اولیه متنوع شامل آزاد شدن اندوتوکسین، فعال شدن سیستم کمپلمان، آسیب ایسکمی- پرفیوژن و طرق دیگر آزاد می شوند.
نتیجه گیریسایتوکین های پیش برنده التهابی و ضد التهابی، حاصل برهم کنش پیچیده غیر قابل پیش بینی آثار سیستم ایمنی بر بدن و حتی اثرات چندگانه در اندام های بدن است. راهبردهای نوین درمانی جاذب سایتوکین ها، راهکاری قوی در تقویت و بهبود خروجی مناسب، متعاقب سندرم پاسخ التهابی سیستمیک هستند.
کلید واژگان: استرس جراحی, سندرم پاسخ التهابی سیستمیک, سایتوکین های پیش برنده التهابی, سایتوکین های ضد التهابیJournal of Shaeed Sdoughi University of Medical Sciences Yazd, Volume:28 Issue: 5, 2020, PP 2614 -2634IntroductionVarious lesions trigger an inflammatory response in the host body. These injuries include surgical stress Surgery exerts stress on the body. Systemic inflammatory syndrome is a reflection of the degree of surgical stress and as a system of assessing the severity of postoperative stress. Regular complexes of inflammatory polypeptide molecules contribute to the development of this inflammatory response known as cytokines. Lack of local control over the release of these cytokines can cause systemic inflammation, and potentially devastating complications.
In writing this review articles, articles indexed in the following databases were used: Science Direct, Scopus, Springer Science, PubMed and Google Scholar Ninety two related research papers, including quantitative and qualitative researches in English, related to the last 40 years (1979- 2019) were included in this study. The current review article has been written based on 92 articles and the keywords of “Surgical Stress, Systemic Inflammatory Response Syndrome, Pro-Inflammatory Cytokines, and Anti-Inflammatory Cytokines”.Studies in humans and animal models suggest that both types of pro-inflammatory and anti-inflammatory cytokines following diverse primary stimuli, including endotoxin release, complement system activation, ischemia-perfusion injury, and other ways.ConclusionInflammatory and anti-inflammatory cytokines are the result of a complex unpredictable interaction of immune system effects on the body and even multiple effects on body organs. New therapeutic strategies for the absorption of cytokines are a powerful way to enhance and improve proper output, following systemic inflammatory response syndrome.
Keywords: Surgical Stress, Systemic Inflammatory Response Syndrome, Pro-Inflammatory Cytokines, Anti-Inflammatory Cytokines -
زمینه و هدف
زنجبیل دارای خواص ضدالتهابی است. هدف از پژوهش حاضر، تعیین پاسخ سایتوکاین های پیش التهابی اینترلوکین-6 (IL-6) و اینترلوکین-8 (IL-8) به مکمل یاری کوتاه-مدت زنجبیل و فعالیت ورزشی وامانده ساز در مردان ورزشکار بود.
روش بررسیدر پژوهشی نیمه تجربی، 40 مرد ورزشکار به چهار گروه 10تایی کنترل، مکمل، فعالیت، مکمل با فعالیت تقسیم شدند. گروه مکمل و مکمل با فعالیت، دو کپسول 500 میلی گرمی پودر زنجبیل را روزانه به مدت یک هفته مصرف کردند. همچنین، گروه فعالیت و مکمل با فعالیت، آزمون بروس را انجام دادند. سطوح پلاسمایی IL-6 و IL-8 قبل و بلافاصله پس از آزمون جمع آوری و اندازه گیری شد. داده ها با آزمون های آماری تی همبسته و آنالیز واریانس یک طرفه تجزیه و تحلیل شد.
یافته هادر مرحله پس آزمون نسبت به پیش آزمون، IL-6 و IL-8 پلاسما در گروه کنترل تغییر معنی داری نیافت (05/0P>)، اما IL-6 و IL-8 پلاسما در گروه فعالیت افزایش معنی-داری و در گروه مکمل و گروه مکمل با فعالیت کاهش معنی داری یافت (05/0P<). همچنین، بین IL-6 و IL-8 پلاسما در چهار گروه تفاوت معنی داری وجود داشت (05/0P<)، به طوری که IL-6 و IL-8 پلاسما در گروه مکمل و مکمل با فعالیت نسبت به گروه کنترل، گروه مکمل نسبت به گروه فعالیت و نیز گروه مکمل با فعالیت نسبت به گروه فعالیت کاهش معنی داری یافت (05/0P<).
نتیجه گیریبه نظر می رسد که مصرف زنجبیل به عنوان یک مکمل مفید ضدالتهابی می-تواند اثر مثبتی بر کاهش سایتوکاین های پیش التهابی IL-6 و IL-8 و در نتیجه بهبود سیستم ایمنی مردان ورزشکار داشته باشد.
کلید واژگان: مکمل یاری, زنجبیل, سایتوکاین پیش التهابی, فعالیت ورزشیBackground and objectiveGinger has anti-inflammatory properties. The purpose of the present study was to determine the response of pro-inflammatory cytokines, interleukin-6 (IL-6), and interleukin-8 (IL-8) to short-term supplementation with ginger and exhaustive exercise in male athletes.
MethodsIn a semi-experimental study, 40 male athletes were divided into 4 groups of control, supplementation, exercise, and supplementation with exercise (10 individuals each). Groups of supplementation and supplementation with exercise took two 500 mg capsules of powdered ginger per day for one week. Participants in exercise and supplementation with exercise groups performed Bruce test. Plasma levels of IL-6 and IL-8 were collected and measured before and immediately after the test. Data was analyzed using paired sample t-test and one-way analysis of variance.
ResultsNo significant difference was found between plasma IL-6 and IL-8 in control group between pretest and posttest (P<0.05); however, plasma IL-6 and IL-8 increased significantly in exercise group and decreased significantly in supplementation and supplementation with exercise groups )P<0.05(. In addition, a significant difference was found between plasma IL-6 and IL-8 in the four groups (P<0.05), so that plasma IL-6 and IL-8 decreased significantly in supplementation and supplementation with exercise groups compared with control group, in supplementation group compared with exercise group, and in supplementation with exercise group compared with exercise group (P<0.05).
ConclusionIt appears that the consumption of ginger, as an anti-inflammatory supplement can have positive effect on the reduction of pro-inflammatory cytokines, IL-6, and IL-8, and thus the improvement of the immune system of male athletes.
Keywords: supplementation, Ginger, pro-inflammatory cytokines, exercise -
BackgroundCalcium sennosides are the main active metabolites of sennas, which have a powerful interest to phytochemical and pharmacological research, due to their brilliant medicinal values. It is well known in folk medicine for their laxative and purgative uses.Materials and MethodsThis experiment aimed to assess cytogenetic (micronucleus assay and chromosomal aberration study) and biochemical effects of calcium sennosides at a working dose (24 or 48 mg/ ml) on suppressing radiation hazards in human blood cultures. Biochemical investigations include superoxide dismutase (SOD), catalase (CAT), tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), cyclooxygenase-2 (COX-2) and lactate dehydrogenase (LDH) levels. The treatment periods were 48 and 72 hrs post-irradiation at a dose of 3 Gy. Triple blood cultures for each blood sample were set up.ResultsIonizing radiation exposure induced significant increase in micronuclei (MN) frequencies in both mono- and bi- nucleated cells, and all types of chromosome aberrations, beside significant decrease in SOD and CAT activities. While TNF-α, IL-8, COX-2 and LDH levels were significantly increased after irradiation. Treatment with calcium sennosides exhibited decreased of micronuclei and chromosome aberration numbers and enhancement in the level of SOD and CAT activities. In addition, a significant amelioration in IL-8, TNF-α, COX-2 levels and LDH activity were scored.ConclusionPresent results revealed the antimutagenic and the anti-inflammatory effects of sennosides against oxidative stress induced by γ- irradiation.Keywords: Calcium sennosides, ?-rays, pro-inflammatory cytokines, micronucleus, chromosomal aberration
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Objective(s)Aberrant expression of CCL5 has been found in several kinds of inflammatory diseases, and the roles of CCL5 in these diseases have also been reported. However, the role of CCL5 in infantile pneumonia is still unclear. Thus, the function and acting mechanism of CCL5 in the in vitro model of infantile pneumonia were researched in this study.Materials And MethodsHuman fetal lung fibroblast WI-38 cells were subjected with lipopolysaccharide (LPS) to mimic an in vitro model of pneumonia. CCL5 was silenced by transfection with CCL5-targeted siRNA, and then cell viability, apoptosis, and the expressions of apoptosis-associated factors were respectively assessed by CCK-8 assay, flow cytometry and Western blot. Besides, expressions of CCL5 and pro-inflammatory factors were analyzed by qRT-PCR and Western blot. The secretions of pro-inflammatory factors were measured by ELISA. Finally, the expressions of main factors in JNK and NF-κB pathways were detected.ResultsLPS treatment suppressed cell viability, promoted cell apoptosis, and enhanced the secretion of IL-6, MCP-1, and TNF-α. Overexpression of CCL5 was found in LPS-treated cells. CCL5 silence protected WI-38 cells from LPS-induced inflammatory damage, with increasing cell viability, inhibiting cell apoptosis, and reducing the production of pro-inflammatory cytokines. Besides, CCL5 silence inhibited LPS-induced activations of JNK and NF-κB pathways.ConclusionDown-regulation of CCL5 could protect WI-38 cells from LPS-induced inflammatory damage via inactivating JNK and NF-κB pathways.Keywords: CCL5, Infantile pneumonia, JNK pathway, Lipopolysaccharide (LPS), NF-κB pathway, Pro-inflammatory cytokines
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IntroductionThe effects of Ramadan observance and any associated dietary restriction upon oxidative stress are not well known. The topic has thus been examined in a brief systematic review of available literature concerning non-athletic but otherwise healthy subjects, patients with selected clinical conditions, and in athletes.MethodsOvid/Medline and Google searches were supplemented by a perusal of reference lists in papers thus identified.ResultsRamadan observance and associated dietary restrictions are generally associated with a decrease of body mass in non-athletic adults, and in patients with conditions such as obesity, metabolic syndrome, diabetes mellitus and hypertension. During Ramadan, measures of oxidative stress (particularly malondialdehyde and F2 isoprostanes) are consistently decreased, antioxidant status (particularly levels of peroxidases, uric acid and reduced glutathione) are enhanced and inflammatory reactions (particularly c-reactive protein, IL-6 and TNF-a) are decreased in association with decreases in body mass. Perhaps because of lower initial body weights and greater dietary control during Ramadan, changes of oxidant status are more variable in athletes; in 3 of 7 studies, Ramadan observance had little effect on oxidant status, and in 2 reports there was some deterioration. In 3 of 4 studies where athletes underwent short-term dieting, there was also no improvement of antioxidant status.ConclusionRamadan observance and any associated dieting reduce oxidative stress in non-athletic individuals, apparently in association with decreases of body mass. In athletes, oxidant levels are generally unchanged during Ramadan, and if food intake is maintained they may even increase. More information is needed upon possible adverse health consequences, but chronic risks are probably small because any changes are limited to one month per year.Keywords: c-reactive 66 protein, F2 isoprostanes, Glutathione, peroxidases, pro-inflammatory cytokines
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