فهرست مطالب aliakbar nekooeian
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Background
Familiarity with and management of drug side effects is among nurses’ main educational needs with respect to pharmacological care in psychiatry departments.
ObjectivesThis study aimed to determine the effects of psychotropic drug education through mobile learning and group discussion on nursing students’ learning, satisfaction, and attitude.
MethodsThis educational intervention was done at EbneSina Psychiatric Hospital, affiliated with Shiraz University of Medical Sciences, in 2018. A total of 28 students were randomly divided into 2 groups, each containing 16 and 12 subjects. The first group underwent the educational intervention through mobile learning. The second group received the educational intervention through group discussion. The students’ learning and satisfaction were assessed and compared before and 2 weeks after the intervention. Attitudes were also assessed within the mobile learning group. Data were analyzed using paired and independent sample t-tests.
ResultsThe results revealed a significant difference in satisfaction between the 2 groups after the intervention (38.69 ± 4.78 in the mobile learning group vs 33.13 ± 5.51 in the discussion group; P = 0.02). However, no significant difference was found after adjustment for baseline, age, and sex. The results also indicated that the students in the mobile learning group developed a significantly more positive attitude after the intervention compared to the baseline (P = 0.038).
ConclusionsThe study findings indicated that the utilization of smartphones for learning about psychotropic drug management in psychiatric departments might be effective in enhancing student’s learning outcomes, satisfaction, and attitude. Thus, further studies with larger sample sizes are recommended to be conducted on other medical and nursing apprenticeships.
Keywords: Mobile Learning, Group Discussion, Psychotropic Drugs} -
مقدمه
تجمع چربی در بافت کبد به عنوان مهم ترین علت بیماری استیاتوهپاتیت غیرالکلی (NASH) شناخته می شود که با کاهش پروتیین گیرنده های فعال تکثیرکننده پراکسی زوم کبدی (PPAR-α) همراه است. این مطالعه با هدف بررسی تاثیر هشت هفته تمرینات تناوبی شنا با شدت بالا (HIST) بر PPAR-α و آنزیم های کبدی در موش های صحرایی NASH ناشی از رژیم غذایی پرچرب (HFD) انجام شد.
روش بررسیتحقیق حاضر از نوع نیمه تجربی بود. 40 سر رت نر نژاد اسپراگوداولی (سن: 6 تا 8 هفته و وزن 20 ± 230 گرم) اختیار شد. سپس به دو گروه مساوی سالم و HFD تقسیم شدند. گروه HFD با هدف القا بیماری، به مدت هشت هفته تحت گاواژ قرار گرفتند. پس از اثبات بیماری، رت ها به چهار گروه کنترل-سالم (9= n)، سالم-شنا (9= n)، کنترل-بیمار (9= n) و بیمار-شنا (9= n) تقسیم شدند. گروه های تمرینی، HIST را هشت هفته (سه جلسه در هفته و هر جلسه 30 دقیقه) انجام دادند. در پایان، PPAR-α کبدی از روش وسترن بلات و آنزیم های ALT) Alanine aminotransferase (AST) Aspartateaminotransferase)و GGT (Gama-Glutamyl Transferase) در سطح سرم از روش فتومتریک اندازه گیری شدند. جهت آنالیز داده ها از آزمون های آماری آنالیز واریانس یک طرفه و آزمون تعقیبی بونفرونی استفاده شد. سطح معنی داری (0/05≥P) و کلیه روش های آماری با استفاده از نرم افزارversion 16 SPSS انجام شد.
نتایجHIST، افزایش وزن ناشی از HFD را کنترل کرد و کاهش معنی دار ALT و AST سرم در گروه های سالم-شنا و بیمار-شنا نسبت به گروه کنترل-بیمار و کاهش معنی دار GGT سرم در سالم-شنا نسبت به کنترل-بیمار (0/001≥P) و بیمار-شنا (0/044≥P) مشاهده شد. افزایش معنی دار PPAR-α کبدی در سالم-شنا نسبت به کنترل-بیمار مشاهده گشت (0/002≥P).
نتیجه گیری:
HIST می تواند وزن بدن را کنترل کند و آنزیم های کبدی را کاهش دهد. با این حال برای حصول نتایج قطعی تحقیقات بیشتری مورد نیاز است.
کلید واژگان: استئاتوهپاتیت غیرالکلی, شنای تناوبی با شدت بالا, پروتئین گیرنده های فعال تکثیرکننده پراکسی زوم کبدی, آنزیم های کبدی}Journal of Shaeed Sdoughi University of Medical Sciences Yazd, Volume:30 Issue: 10, 2023, PP 6034 -6051IntroductionAccumulation of fat in the liver tissue is known as the most important cause of non-alcoholic steatohepatitis, which is associated with a decrease in the protein of hepatic peroxisome proliferator-activated receptors (PPAR-α). This study aimed to investigate the effect of eight weeks of high-intensity interval training (HIST) on PPAR-α and liver enzymes in high-fat diet-induced non-alcoholic steatohepatitis rats.
MethodsThe current research was semi-experimental. 40 Spraguedauli male rats (age: 6 to 8 weeks and weight: 230 ± 20 grams) were selected and divided into two equal groups, healthy and high-fat diet (HFD). The HFD group was subjected to gavage for eight weeks with the aim of inducing the disease. Rats were divided into four groups: control-healthy (n=9), healthy-swimming (n=9), control- disease (n=9) and disease -swimming (n=9). The training groups performed HIST for eight weeks (three sessions per week, each session lasting 30 minutes). In the end, liver PPAR-α was measured by western blot analysis; and ALT, AST and GGT enzymes in serum level were measured by photometric method. One-way analysis of variance and Bonferroni's post hoc test were used to analyze the data. Significant level (P≥0.05) and all statistical methods were performed using SPSS16 software.
ResultsHIST controlled the weight gain caused by HFD and there was a significant decrease in serum ALT and AST in the healthy-swimming and sick-swimming groups compared to the control-patient group and a significant decrease in serum GGT in the healthy-swimming group compared to the control-patient (P≤0.001) and patient-swimming (P≤0.044) were observed. A significant increase in hepatic PPAR-α was observed in healthy-swimming patients compared to the control-patients (P≤0.002).
ConclusionHIST can control body weight and reduce liver enzymes. However, more research is needed to obtain definitive results.
Keywords: Non-alcoholic Steatohepatitis, High-intensity Interval Swimming, Hepatic peroxisome proliferator activator protein, Liver enzymes} -
Background
Captopril, an angiotensin-converting enzyme inhibitor, and losartan, an angiotensin II receptor blocker, are used for the treatment of hypertension, but their effects on cardiac stereology are unknown. This study, therefore, aimed to examine their effects on cardiac stereology in rats with renovascular hypertension.
MethodsThis study was conducted at Histomorphometry and Stereology Research Centre, and Cardiovascular Pharmacology Research Lab, Department of Pharmacology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran, in August 2015 to August 2016. Fourty-eight rats were allocated to six groups (n=8 per each group): a sham group, which received a vehicle (distilled water) and five renal artery-clipped groups, which received the vehicle, captopril (50 or 100 mg/kg/day), or losartan (25 or 50 mg/kg/day). After four weeks, the animals’ systolic blood pressures (mm Hg) were measured, and the total volumes of their heart, myocardium, endocardium, matrix, and myocardial vessels (mm3), as well as the number of their cardiomyocytes, and Purkinje fibers were determined. Data were analyzed using one-way analysis of variance (ANOVA) followed by least significant difference (LSD) test. P value of equal to or less than 0.05 was considered significant.
ResultsThe renal artery-clipped rats receiving the vehicle had a significantly higher systolic blood pressure (p <0.001); heart weight (g) (p <0.001); and total volume of the heart (p <0.001), myocardium (P=0.020), endocardium (P=0.009), and myocardial vessels (P=0.008); as well as a significantly lower number of cardiomyocytes (P=0.010) and Purkinje cells (P=0.005), than did the rats in the sham group. The renal artery-clipped rats receiving captopril or losartan had a significantly lower systolic blood pressure (p <0.001), heart weight (P=0.007), and total volume of the heart (p <0.001), myocardium (p <0.001), endocardium (P=0.027), and myocardial vessels (P=0.004) than did the renal artery-clipped rats receiving the vehicle. Neither captopril nor losartan prevented a reduction in the number of Purkinje cells, but captopril at the higher dose attenuated cardiomyocyte loss (P=0.010).
ConclusionCaptopril and losartan lowered the systolic blood pressure and cardiac hypertrophy but failed to prevent Purkinje cell loss. Captopril only at the higher dose prevented cardiomyocyte loss. Captopril exerted a greater inhibitory effect on cardiac stereology, which warrants further research.
Keywords: Heart, Hypertension, Renovascular, Captopril, Losartan} -
BackgroundLiposomes constitute a promising drug delivery vehicle, and are believed to improve drugs’ effectiveness. This study was aimed to compare antihypertensive and vascular modifying activities of liposomal and non-liposomal forms of ascorbic acid.MethodsForty-nine male Sprague-Dawley rats were randomly divided into seven groups (n=7): A sham vehicle-receiving (Sham-veh), hypertensive (HTN), vehicle-receiving hypertensive (HTN-Veh), two liposomal Ascorbic acid-treated hypertensive at 50 or 100 mg/kg/day (LVC-50 and LVC-100), and two non-liposomal Ascorbic acid-treated hypertensive at 50 or 100 mg/kg/day (VC-50 and VC-100). Systolic blood pressure (SBP) and heart rate (HR) were measured weekly; after 4 weeks, dose-responses to phenylephrine (PE) in the absence and presence of nitro-L-arginine methyl ester (L-NAME), acetylcholine (Ach), and sodium nitroprusside (SNP) were obtained on aortic rings. Data were analyzed with one-way ANOVA and Duncan’s multiple range test at a P value of <0.05 using Sigmastat statistical software.ResultsCompared to the non-liposomal form, the liposomal one was associated with more prominent effects on the final SBP. Both forms of Ascorbic acid decreased SBP dose-dependently. The basal and stimulated release of Nitric Oxide (NO) was significantly recovered by both forms of Ascorbic acid. The PE maximal responses were not significantly different between the liposomal and non-liposomal groups (P=0.08). Although the Emax of Ach-relaxation response was not different in two preparation forms, Ach-relaxation response induced a lower concentration of the liposomal form of Ascorbic acid (P=0.03)ConclusionThe liposomal Ascorbic acid exhibited relaxation activity in significantly lower concentrations. The observed effects were partly mediated by the increased basal release of NO.Keywords: liposomes, Ascorbic Acid, Rats, Hypertension, Nitric oxide}
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BackgroundUlcerative colitis is an inflammatory disease with indefinite treatment. The present study aimed to assess the anti-inflammatory and antioxidant effects of Carum copticum L. (CC) extract on induced colitis in rats.MethodsSixty male rats were randomly divided into six groups (n=10 per group). Acetic acid-induced colitis rats were orally administered with doses of 100, 200, and 400 mg/kg CC extract, and 100 mg/kg sulfasalazine for seven consecutive days, respectively. Colonic biopsies were taken to measure histopathological parameters as well as the tumor necrosis factor (TNF-α), interleukin-6 (IL-6), myeloperoxidase (MPO), malondialdehyde (MDA), and glutathione (GSH). Data analysis was performed using the one-way ANOVA and Tukey’s test for normally distributed data. Kruskal-Wallis test followed by Dunn’s test was used for non-normally distributed data. The analysis was performed at P≤0.05 using SigmaStat software (version 10.0).ResultsThe control colitis group had a significantly higher total colitis index (P=0.01), TNF-α (P=0.01), IL-6 (P=0.01), MPO (P=0.01), and MDA (P=0.01); and lower GSH (P=0.01) than those of the sham group. The colitis group receiving a dose of 200 mg/kg/day CC extract had a significantly lower total colitis index (P=0.01), TNF-α (P=0.01), IL-6 (P=0.01), MPO (P=0.01), and MDA (P=0.01); and higher GSH (P=0.01) than those of the control colitis group. The colitis group receiving a dose of 200 mg/kg/day CC extract had a significantly lower total colitis index (P=0.04), TNF-α (P=0.03), IL-6 (P=0.04), MPO (P=0.03), and MDA (P=0.03); and higher GSH (P=0.01) than those of the colitis group receiving sulfasalazine.ConclusionThe present study revealed that CC extract had healing effects on colitis, possibly due to its antioxidant and anti-inflammatory properties.Keywords: Colitis, Ulcerative, Rats, Cytokines, Antioxidants, Anti-Inflammatory agents}
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BackgroundRat model of chronic myocardial infarction and heart failure is associated with endothelial dysfunction, which has partly been attributed to increased oxidative stress.ObjectivesThis study aimed to examine the effects of oleuropein on vascular endothelial dysfunction in rats with chronic myocardial infarction.Materials And MethodsThe rats were subjected to coronary artery ligation or sham operation. On the next day, they were divided into a sham and a coronary-ligated group receiving distilled water (1 mL/day) and two coronary artery-ligated groups receiving 10 or 20 mg/kg/day oleuropein. Five weeks later, hemodynamic variables were measured, isolated aortic studies were performed, and serum concentrations of superoxide dismutase and malondialdehyde were determined. The data were entered into Sigmastat Statistical Software and were analyzed using one-way ANOVA followed by Duncans Multiple Range. P ≤ 0.05 was considered to be statistically significant.ResultsThe rats with myocardial infarction receiving vehicle had a significantly lower left ventricular systolic pressure (P = 0.04), rate of rise (P = 0.03), decrease of left ventricular pressure (P = 0.03), relaxation response to acetylcholine (P = 0.01), and serum levels of superoxide dismutase (P = 0.01). Oleuropein treatment prevented the reduction of these variables. Moreover, the myocardial infarction group receiving vehicle had a significantly higher contraction response to phenylephrine (P = 0.03) and serum levels of malondialdehyde (P = 0.02) compared to the sham group. Treatment with oleuropein prevented the increase of these variables. There was no significant difference among the study groups regarding heart rate.ConclusionsThe findings indicated that chronic myocardial infarction resulted in heart failure and was associated with endothelial dysfunction. They also demonstrated that oleuropein attenuated endothelial dysfunctions, possibly, by antioxidative effects.Keywords: Oleuropein, Rats, Oxidative Stress}
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BackgroundResveratrol has beneficial effects on experimental and clinical hypertension and diabetes.ObjectivesThis study aimed at examining antidiuretic and antihyperlipidemic effects of resveratrol in rats with simultaneous type II diabetes and endovascular hypertension.Materials And MethodsThis study was performed on eight groups of male SpargueDawley rats each containing 8 - 10 animals as follows: control, diabetic (induced by streptozotocin and nicotinamide), renovascular hypertensive (induced by placing Plexiglas clips on the left renal arteries), sham, simultaneously hypertensivediabetic receiving vehicle (distilled water), and 3 simultaneously hypertensive-diabetic groups receiving 5, 10, and 20 mg/kg/day resveratrol. Blood pressure and heart rate were measured weekly and fasting blood glucose, serum cholesterol, triglyceride, and markers of oxidative stress were measured after 4 weeks of treatment with resveratrol vehicle. The data were analyzed using one-way Analysis of Variance (ANOVA) and Duncans multiple range tests. Data analysis was done using SigmaStat software and P ≤ 0.05 was considered to be statistically significant.ResultsSerum malondialdehyde, systolic blood pressure, heart rate, fasting blood glucose, blood glycated hemoglobin, and serum triglyceride, total cholesterol, and low-density lipoprotein cholesterol levels were significantly higher in the hypertensivediabetic group receiving vehicle compared to the control group (PConclusionsThe findings indicated that resveratrol had antidiabetic, antihypertensive, and antihyperlipidemic effects, which might be partly due to an antioxidant mechanism.Keywords: Resveratrol, Diabetes, Renovascular Hypertension, Oxidative Stress, Rat}
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Changes in the substitutions at C-3 and C-5 positions of 4-(1-methyl-5-nitro-2-imidazolyl) dihydropyridine analogs of nifedipine have led to changes in potency of the compounds. The objective of the present study was to examine the hypotensive effects of 5 newly synthesized dihydropyridine derivatives of nifedipine in rats with phenylephrine-raised blood pressure. Anesthetized Sprague-Dawley rats were randomly assigned to 19 groups of 7 animals each. Control group received the vehicle dimethylsulfoxide (0.05 mL), 3 groups were given nifedipine at 100, 300, or 1000 mg/kg, and 5 other groups each composed of 3 subgroups administered one of the 5 new dihydropyridine compound at 100, 300, or 1000 mg/kg. All animals were initially infused with 20 µg/kg/min phenylephrine for 45 min, and were then given a bolus of either dimethylsulfoxide, nifedipine, or new dihydropyridine compounds 20 min after the commencement of phenylephrine infusion. Blood pressure and heart rate (HR) of the animals were measured before and at the end of phenylephrine infusion, or 25 min after injection of vehicle or compounds. Compared to dimethylsulfoxide, nifedipine, and new 1, 4-dihydropyridine derivatives caused significant reductions in MBP. Moreover, cyclohexyl propyl, phenyl butyl, and cyclohexyl methyl analogs of 1, 4-dihydro-2,6-dimethyl-4-(1-methyl-5-nitro-2-imidazoyl)-3,5-pyridinedicarboxylase at 100 mg/kg, phenyl butyl, and cyclohexyl methyl analogs at 300 mg/kg, and cyclohexyl methyl analogs at 1000 mg/kg reduced MBP similar to nifedipine. There was no significant difference between HR of all groups before and after administration of the compounds. The findings indicated that changes in substitution at C-3 and C-5 positions of 2-(1-methyl-5-nitro-2-imidazolyl) dihydropyridine analogs of nifedipine were associated with changes in hypotensive activity of the compounds.Keywords: 1, 4, dihydropyridine, Nifedipine, Phenylephrine, Arterial pressure}
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Objective(s)Theneuroprotective effect of lithium has been attributed to its therapeutic action. However, the role of glial cells particularly astrocytes, and the possible interactions between neurons and astrocytes in neuroprotective effects of lithium have been disregarded. Thus, the aim of this study was to evaluate the direct effects of lithium on brain derived neurotrophic factor (BDNF) and glial cell line derived neurotrophic factor (GDNF) in rat primary neuronal, astrocytes, and mixed neuro-astroglial cultures to assess the possible effects of lithium on astrocytes and neuro-astroglia interactions.Materials And MethodsRat primary astrocyte, neuronal and mixed neuro-astrocyte cultures were prepared from cortices of 18-day embryos. Cell cultures were exposed to lithium (1 mM) or vehicle for 1 day (acute) or 7 days (chronic). BDNF and GDNF mRNA and protein levels were determined by RT-PCR and ELISA, respectively.ResultsChronic but not acute lithium treatment increased intracellular BDNF and GDNF protein levels in rat primary neuronal and astrocyte cultures, respectively (P<0.05). However, chronic lithium treatment had no significant effect on intracellular BDNF protein level in astrocyte and mixed neuron-astrocyte cultures or GDNF protein levels in mixed neuron-astrocyte culture. Furthermore, acute and chronic lithium treatment had no significant effect on mRNA and extracellular BDNF and GDNF protein levels in three studied cultures.ConclusionPresent study showed that chronic lithium treatment affected neurotrophins both in neurons and astrocytes in a cell-type specific manner with no effect on neuron-astrocyte interactions. The findings of this study also highlighted the importance of astrocytes as drug targets involved in the neuroprotective action of lithium.Keywords: Astrocytes, BDNF, Culture, GDNF, Lithium, Neuro, astroglial, Neurons}
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S100ß a neurotrophic factor mainly released by astrocytes, has been implicated in the pathogenesis of bipolar disorder. Thus, lithium may exert its neuroprotective effects to some extent through S100ß. Furthermore, the possible effects of lithium on astrocytes as well as on interactions between neurons and astrocytes as a part of its mechanisms of actions are unknown. This study was undertaken to determine the effect of lithium on S100β in neurons, astrocytes and a mixture of neurons and astrocytes. Rat primary astrocyte, neuronal and mixed neuro-astroglia cultures were prepared from cortices of 18-day''s embryos. Cell cultures were exposed to lithium (1mM) or vehicle for 1day (acute) or 7 days (chronic). RT-PCR and ELISA determined S100β mRNA and intra- and extracellular protein levels. Chronic lithium treatment significantly increased intracellular S100β in neuronal and neuro-astroglia cultures in comparison to control cultures (P<0.05). Acute and chronic lithium treatments exerted no significant effects on intracellular S100β protein levels in astrocytes, and extracellular S100β protein levels in three studied cultures as compared to control cultures. Acute and chronic lithium treatments did not significantly alter S100β mRNA levels in three studied cultures, compared to control cultures. Chronic lithium treatment increased intracellular S100ß protein levels in a cell-type specific manner which may favor its neuroprotective action. The findings of this study suggest that lithium may exert its neuroprotective action, at least partly, by increasing neuronal S100ß level, with no effect on astrocytes or interaction between neurons and astrocytes.Keywords: Lithium, S100β Astrocytes, Neurons, Primary cell culture}
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BackgroundResveratrol has beneficial effects on cardiovascular system. This study aimed at examining antidiabetic and antihypertensive effects of resveratrol in rats with simultaneous type 2 diabetes and renal hypertension.MethodsEight groups (8-10 each) of male Spargue-Dawley rats, including a control, a diabetic (induced by streptozotocin and nicotinamide), a renal hypertensive (induced by placing plexiglas clips on the left renal arteries), a sham, a simultaneously hypertensive-diabetic receiving vehicle, and 3 simultaneous hypertensive-diabetic receiving resveratrol at 5, 10 or 20 mg/kg/day were used. Four weeks after the induction of diabetes, renal hypertension was induced and animals were given vehicle or resveratrol for the next four weeks. Afterwards, blood pressure and glucose, serum markers of oxidative stress were measured and animal’s aortic rings were used for isolated studies.ResultsSerum malondialdehyde, systolic blood pressure, heart rate, fasting blood glucose, maximal response and effective concentration 50 of phenylephrine, and inhibitory concentration 50 of acetylcholine of hypertensive-diabetic group receiving vehicle were significantly higher than those of the control group, and treatment with resveratrol caused significant reduction of these variables. Moreover, serum superoxide dismutase, glutathione reductase, and maximal response to acetylcholine of hypertensive-diabetic group receiving vehicle were significantly lower than those of the control group, and treatment with resveratrol caused significant increase of these variables.ConclusionThe findings indicate that resveratrol has antidiabetic and antihypertensive effects, which may be partly due to antioxidant mechanism. They also show that antihypertensive effect of resveratrol may be additionally mediated by improving the release of nitric oxide and sympathoplegic activities.
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BackgroundSome species of Allium family are known to have antihypertensive, anti-diabetic, and lipid lowering effects..ObjectivesThis study aimed to examine the possible mechanisms of antihypertensive, anti-diabetic, and anti-lipid activities of Allium eriophyllum which grows in Fars province, Iran in a rat model of simultaneous type 2 diabetes and renal hypertension..Materials And MethodsThis study was conducted on six groups of male Spargue-Dawley rats each containing 8 - 10 animals, including a sham-control, a diabetic, a renal hypertensive, and three simultaneously hypertensive–diabetic groups receiving vehicle or 30 or 100 mg/kg/day hydroalcoholic extract of Allium eriophyllum. Four weeks after induction of diabetes, renal hypertension was induced and the animals started receiving the vehicle or extract for the subsequent four weeks. Afterwards, blood pressure, fasting blood sugar, serum cholesterol, triglyceride, and markers of oxidative stress were measured, and isolated studies were performed on aortic rings..ResultsSystolic blood pressure, heart rate, fasting blood sugar, maximal response, and effective concentrations 50 (EC50) of phenylephrine and acetylcholine of the hypertensive-diabetic group receiving vehicle were significantly higher compared to those of the sham-control group, and treatment with the extract led to a significant reduction in these variables. Moreover, serum superoxide dismutase and glutathione reductase and maximal response of acetylcholine were significantly lower in the hypertensive-diabetic group receiving vehicle in comparison to the sham-control group, and treatment with the extract significantly reduced these variables..ConclusionsThe present study findings indicated that antihypertensive, anti-diabetic, and anti-lipid effects of the extract might be partly due to its antioxidant mechanism. It was also revealed that its antihypertensive effects may be additionally mediated by improving the release of nitric oxide as well as by sympatholytic activities..Keywords: Diabetes, Renal Hypertension, Oxidative Stress, Rats}
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پیشزمینهآنژیوتانسین دو نقش مهمی در تنظیم جریان خون موضعی در مغز دارد اما نقش مستقیم آن در بروز ادم ایسکمیک مغزی روشن نیست. این مطالعه با استفاده از کندسارتان به عنوان یک آنتاگونیست گیرنده های AT1، نقش آنژیوتانسین دو مرکزی در آسیب سد خونی - مغزی ناشی از ایسکمی – ریپرفیوژن و ایجاد ادم مغزی را در موش صحرایی مورد بررسی قرار می دهد.روش هادوره ایسکمی در حیوانات مورد مطالعه با انسداد شریان میانی مغز به مدت 60 دقیقه ایجاد شد. تزریق داخل وریدی دوز غیر موثر بر فشار خون کندسارتان 1/ میلی گرم بر کیلوگرم و حلال آن در گروهای مورد مطالعه یک ساعت قبل از ایجاد ایسکمی انجام شد. 24 ساعت پس از پایان ایسکمی حیوانات از نظر اختلالات حرکتی مورد ارزیابی قرار گرفتند. پس از آن زیر بیهوشی عمیق سر حیوانات جدا شده و بافت مغز خارج شده و جهت ارزیابی حجم ضایعه مغزی، ادم و نفوذپذیری سد خونی – مغزی مورد استفاده قرار گرفت.نتایجوقوع 24 ساعت ریپرفیوژن به دنبال 60 دقیقه ایسکمی در مغز سبب ایجاد اختلالات حرکتی شدید، آسیب قابل ملاحظه سد خونی – مغزی (نشت اوانس بلو به میزان 1/94 ± 12/5 میکروگرم بر گرم)، ادم مغزی به میزان 4/02 درصد و ضایعه مغزی به میزان 21 ± 317 میلیمتر مکعب شد. تجویزکندسارتان با دوز 0/1 میلی گرم بر کیلوگرم بدون تغییر فشار خون علاوه بر بهبود اختلالات حرکتی نشت سد خونی – مغزی را به میزان 54/9 درصد، ادم مغزی را به میزان 59/2 درصد و ضایعه مغزی را به میزان 54/9 درصد کاهش داد.نتیجه گیریمهار گیرنده های AT1 آنژیوتانسین دو بدون کاهش فشار خون، عروق مغزی را در برابر آسیب ناشی از سکته مغزی محافظت می کند.
کلید واژگان: سد خونی - مغزی, ادم مغزی, گیرنده های AT1, کندسارتان}BackgroundAngiotensin II (Ang II) has an important role on cerebral microcirculation; however, its direct roles in terms of ischemic brain edema need to be clarified. This study evaluated the role of central Ang II by using candesartan, as an AT1 receptor blocker, in the brain edema formation and blood-brain barrier (BBB) disruption caused by ischemia/reperfusion (I/R) injuries in rat.MethodsRats were exposed to 60-min middle cerebral artery (MCA) occlusion. Vehicle and non-hypotensive doses of candesartan (0.1 mg/kg) were administered one hour before ischemia. Neurological dysfunction scoring was evaluated following 24 h of reperfusion. Animals were then decapitated under deep anesthesia for the assessments of cerebral infarct size, edema formation, and BBB permeability.ResultsThe outcomes of 24 h reperfusion after 60-min MCA occlusion were severe neurological disability, massive BBB disruption (Evans blue extravasation = 12.5 ± 1.94 µg/g tissue), 4.02% edema, and cerebral infarction (317 ± 21 mm3). Candesartan at a dose of 0.1 mg/kg, without changing arterial blood pressure, improved neurological dysfunction scoring together with significant reductions in BBB disruption (54.9%), edema (59.2%), and cerebral infarction (54.9%).ConclusionsInactivation of central AT1 receptors, if not accompanied with arterial hypotension, protected cerebral micro-vasculatures from damaging effects of acute stroke.Keywords: Blood–brain barrier, Brain edema, AT1 receptor, Candesartan} -
زمینه و هدفسکته مغزی سومین عامل مرگ و معلولیت در جوامع صنعتی است. پیشنهاد شده است که سیستم رنین- آنژیوتانسین ممکن است در مکانیسمهای پاتولوژیک سکته مغزی نقش داشته باشد. هدف از این مطالعه بررسی اثرات درمانی مهار گیرنده های AT1 آنژیوتانسین دو بر ضایعه ایسکمیک مغزی می باشد. این مطالعه با استفاده از مدل آزمایشگاهی ایسکمی موضعی مغز در موش صحرایی با فشار خون طبیعی انجام شده است.روش کاردر این تحقیق تعداد 48 عدد موش صحرایی نر از نژاد Sprague - Dawley درچهارگروه مورد مطالعه قرار گرفتند.گروه شاهد، گروه کنترل ایسکمیک و و دو گروه ایسکمیک که داروی کندسارتان را (با دوزهای 1/0 میلی گرم بر کیلوگرم یا 5/0 میلی گرم بر کیلوگرم) در آغاز مرحله برقراری مجدد جریان خون پس از وقوع ایسکمی دریافت کردند. ایسکمی موضعی با استفاده از تکنیک انسداد شریان میانی مغز توسط فیلامان مخصوص در نیمکره راست مغز حیوانات به مدت یک ساعت ایجاد شد. در این حیوانات 24 ساعت پس از پایان ایسکمی اختلالات حرکتی با استفاده از آزمون نورولوژیک ویژه ای ارزیابی شد وحجم ضایعه مغزی ایجاد شده با استفاده از تکنیک رنگ آمیزی با تری فنیل تترازولیوم کلرایدتعیین شد.یافته هاحیوانات گروه شاهد عملکرد حرکتی طبیعی داشتند (نمره آزمون نورولوژیک 1) و آسیب ایسکمیک در نواحی قشری و زیر قشری مغز آنها مشاهده نشد. وقوع ایسکمی در گروه کنترل سبب ایجاد حجم ضایعه قابل ملاحظه ای در قشر مغز (15 ± 253 میلیمترمکعب) و نواحی زیر قشری (7 ± 92 میلیمتر مکعب) شد و حیوانات این گروه اختلالات حرکتی شدیدی داشتند. مهار گیرنده های AT1 آنژیوتانسین دو با داروی کندسارتان (با دوزهای 1/0 میلی گرم بر کیلوگرم یا 5/0 میلی گرم بر کیلوگرم) اختلالات حرکتی ناشی از ایسکمی را کاهش داد و حجم ضایعه مغزی را در نواحی قشری و زیر قشری مغز بطور معنی داری کاهش داد.نتیجه گیرییافته های این مطالعه نشان می دهد که آنژیوتانسین دو از طریق تحریک گیرنده های AT1 در ایجاد ضایعه ایسکمیک مغزی نقش دارد. و مهار این گیرنده ها می تواند حجم ضایعه ایسکمیک مغزی را کاهش داده و اختلالات حرکتی ناشی از سکته مغزی را بهبود ببخشد.
کلید واژگان: سکته مغزی, گیرنده های AT1, کندسارتان, موش صحرایی}Background and ObjectivesIschemic stroke remains the third leading cause of invalidism and death in industrialized countries. It is suggested that renin–angiotensin system (RAS) may contribute in stroke related pathogenic mechanisms and involve in the ischemic brain damage. This study designed to investigate the role of angiotensin II (Ang II) in conjunction with AT1 receptors in treatment of the brain injuries following transient focal cerebral ischemia in rats.MethodsForty eight male Sprague-Dawley rats were studied in four groups. Sham group, ischemic control group and two ischemic groups that received candesartan (0.1mg/kg, or 0.5mg/kg) at the beginning of reperfusion period. Transient focal cerebral ischemia was induced by 60 minutes occlusion of the middle cerebral artery, followed by 24 hours reperfusion. At the end of the reperfusion period, neurological deficit score (NDS) was performed. Total cortical and striatal infarct volumes were determined using triphenyltetrazolium chloride (TTC) staining technique.ResultsAnimals in sham operated group had normal motor function and no ischemic lesions were observed in cortical or striatal regions. Occurring ischemia in ischemic control group that received vehicle produced considerable infarction in cortex (253±15mm3) and striatum (92±7mm3), as well as these animals had sever impaired motor dysfunctions. Blocking of AT1 receptors with candesartan (0.1mg/kg or 0.5mg/kg) improved neurological outcome and significantly lowered cortical and striatal infarct volumes relative to ischemic control group.ConclusionThe findings of the present study indicated that stimulation of AT1 receptors by Ang II involved in ischemia/reperfusion injuries and blocking of AT1 receptors can decrease ischemic brain injury and improve neurological outcome.Keywords: Stroke, AT1 Receptor, Candesartan, Rat} -
BackgroundPomegranate seed oil and its main constituent, punicic acid, have been shown to decrease plasma glucose and have antioxidant activity. The objective of the present study was to examine the effects of pomegranate seed oil on rats with type 2 diabetes mellitus.MethodSix groups (n=8 each) of male Sprague-Dawley rats, comprising a control, a diabetic (induced by Streptozocin and Nicotinamide) receiving water as vehicle, a diabetic receiving pomegranate seed oil (200 mg/kg/day), a diabetic receiving pomegranate seed oil (600 mg/kg/day), a diabetic receiving soybean oil (200 mg/kg/day), and a diabetic receiving soybean oil (600 mg/kg/day), were used. After 28 days of receiving vehicle or oils, blood glucose, serum levels of insulin, malondialdehyde, glutathione peroxidase, and lipid profile were determined.ResultsThe diabetic rats had significantly higher levels of blood glucose, serum triglyceride, low-density lipoprotein cholesterol, total cholesterol, and malondialdehyde and lower levels of serum insulin and glutathione peroxidase. Rats treated with pomegranate seed oil had significantly higher levels of serum insulin and glutathione peroxidase activity, and there were no statistically significant differences in terms of blood glucose between them and the diabetic control group.ConclusionThe findings of the present study suggest that pomegranate seed oil improved insulin secretion without changing fasting blood glucose.
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BackgroundThe cardiac effects simultaneously occurring during experimental hypertension and diabetes have rarely been investigated. This study aimed at examining the effects of short-term renovascular hypertension and type 2 diabetes on cardiac functions.MethodsFive groups (7 each) of male Sprague-Dawley rats, including a control group, a diabetes (induced by Streptozocin and Nicotinamide) group, a renovascular hypertensive (induced by placing Plexiglas clips on the left renal arteries) group, a sham group, and a simultaneously hypertensive-diabetic group, were used. The animals’ hearts were used for isolated heart studies, and the indices of cardiac functions and coronary effluent creatine kinase MB were measured. The results were analyzed using One-way Analysis of Variance, followed by the Duncan Multiple Range test.ResultsThe diabetic group had a significantly lower rate of rise (-29.5%) and decrease (-36.18%) in ventricular pressure, left ventricular developed pressure (-28.8%), and rate pressure product (-35%), and significantly higher creatine kinase MB (+166%) and infarct size (+36.2%) than those of the control group. The hypertensive group had a significantly higher rate of rise (+12.17%) and decrease (+16.2%) in ventricular pressure, left ventricular developed pressure (+16%), and rate pressure product (+24%), and significantly lower creatine kinase MB (-30%) and infarct size (-27%) than those of the sham group. Simultaneously, the diabetic and hypertensive rats had a significantly higher rate of rise (+32%) and decrease (+30.2%) in ventricular pressure, left ventricular developed pressure (+17.2%), and rate pressure product (+22.2%), and significantly lower creatine kinase MB (-24%) and infarct size (-16.2%) than those of the diabetic group.ConclusionThe findings indicated that the simultaneity of hypertension with type 2 diabetes attenuated diabetes-induced cardiac impairment.
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Journal of Advances in Medical Education & Professionalism, Volume:1 Issue: 4, Oct 2013, PP 113 -118IntroductionGraduate (PhD) students in medical sciences, who will form future faculties and investigators in Iran’s Universities of Medical Sciences, are not trained on scientific writing during their training. The present study describes the design, implementation, and evaluation of Principles of Writing Biomedical Research Paper course.MethodsThe course, prepared based on an extensive search of the literature and books on writing biomedical research papers, was offered as an elective course to PhD students at Shiraz University of Medical Sciences in the second semester of 2011-2012 academic year. The structure and function of various sections of a paper and publication ethics were discussed in lecture and practical sessions over a period of 12 weeks. The course was then evaluated using a self-designed questionnaire.ResultsThe majority of students gave the highest score (20) to the content and implementation of all sessions of the course. Moreover, most of them believed that the allotted time to the course was not enough, and suggested that it should be increased to 32 hours (equal to two credits). Also, almost all the participants believed that overall the materials lectured were comprehensive, the practical sessions were important in learning the lectured materials, and the course was useful in advancing their abilities and skills to write papers.ConclusionThe evaluation of the present course showed that it was able to increase the participants’ knowledge of the structure of scientific papers, and enhanced their abilities and skills to write papers. The evaluation was used as a basis to modify the course.Keywords: Design, Evaluation, Biomedical, Principles of writing}
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BackgroundB cell CLL/lymphoma 2 protein, bcl-2, is an important anti-apoptotic factor that has been implicated in lithium’s neuroprotective effect. However, most studies have focused on assessing the effects of lithium in neurons, ignoring examination of bcl-2 in astrocytes, which also influence neuronal survival and are affected in bipolar disorder. The aim of this study was to evaluate whether chronic lithium treatment also elevates bcl-2 expression in astrocytes compared with neuronal and mixed neuron-astrocyte cultures.MethodsRat primary astrocyte, neuronal, and mixed neuron-astrocyte cultures were prepared from the cerebral cortices of 18-day embryos. The cell cultures were treated with lithium (1 mM) or vehicle for 24 h or 7 days. Thereafter, bcl-2 mRNA and protein levels were determined by RT-PCR and ELISA, respectively.ResultsChronic, but not acute, lithium treatment significantly increased bcl-2 protein levels in the astrocyte cultures compared with the vehicle-treated cultures. While lithium treatment increased bcl-2 protein levels in both neuronal and mixed neuron-astrocyte cultures, the elevations fell short of statistical significance compared with the respective vehicle-treated cultures. However, neither acute nor chronic lithium treatment affected bcl-2 mRNA levels in any of the three cell types studied.ConclusionIncreased bcl-2 levels in rat primary astrocyte cultures following chronic lithium treatment suggest astrocytes are also a target of lithium’s action. In light of the evidence showing decreased numbers of glial cells in the post-mortem brain of patients bipolar disorder with and increased glial numbers following lithium treatment, the findings of this study indicate that lithium’s action on astrocytes may account, at least in part, for its therapeutic effects in bipolar disorder.
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According to Iran’s folk medicine, camphor, a crystalline ketone obtained from essential oils of Cinnamomum camphora, has both sexual behavior attenuating and enhancing properties. This study examined the effects of camphor on sexual behavior in male rats. Twenty four sexually mature male Sprague-Dawley rats were randomly divided into 4 groups receiving daily i.p. injections of olive oil as vehicle (2.5 ml/kg) or camphor at 2.5, 12.5 or 50 mg/kg for 7 days. Afterwards, mount latency (ML), mount frequency (MF), intromission latency (IL) and intromission frequency (IF) of male rats in the presence of sexually receptive females rats were recorded. There was no significant difference in MF or IF from control and experimental groups. However, at the 50 mg/kg dose, camphor reduced the ML and IL relative to that of control rats. The finding indicates that at this dose, camphor had sexual desire and sexual performance enhancing properties.Keywords: camphor, Intromission latency, Mount latency, Sexual behavior}
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The influenza viruses are major etiologic agents of human respiratory infections, and inflict a sizable health and economic burden. This study examines the antiinfluenza virus activity of hydroalcoholic extract of olive leaves (OLHE). Olive leaves were collected from gardens around the city of Shiraz, characterized, dried, ground to powder, and its hydroalcoholic extract was prepared. The influenza viruses were isolated from patients and characterized by standard antiinfluenza sera.Virucidal effects of OLHE (10-1 to 103 μg/ml) were examined in pretreatment, treatment and incubation protocols using quantal assay after incubation for 72 h. All experiments were performed three times in quadruplicates. Pretreatment of the cell line with OLHE for one hour followed by the addition of the virus was associated with virucidal effects (1 to 1000 μg/ml). OLHE added one hour after incubation of the virus with cell did not show antiviral effects. OLHE incubated with the virus for one hour, and then added to the cell line did have antiviral activity (1to 1000 μg/ml). The findings indicate that antiviral activity of OLHE occurred extra-cellularly, probably by changing the properties of membrane of the virus, rather than that of the cell, to prevent the virus from attaching and penetrating the cell line.Keywords: Influenza virus, MDCK cell line, Olive leaf}
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