Exercise Physiology
Fateme Mokhtari; Elahe Talebi Garakani; Khadije Nasiri; Abolfazl Akbari
Abstract
Objectives: The purpose of this study was to evaluate the effect of continuous and high intensity interval training with silymarin consumption on liver enzymes and histological modifications in rats with dexamethasone-induced nonalcoholic fatty liver disease.Method: Male rats were initially divided into ...
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Objectives: The purpose of this study was to evaluate the effect of continuous and high intensity interval training with silymarin consumption on liver enzymes and histological modifications in rats with dexamethasone-induced nonalcoholic fatty liver disease.Method: Male rats were initially divided into 2 groups: normal and exposed to dexamethasone. Dexamethasone group were randomly divided into 6 groups. control (C), Silymarin (S), continues training (CT), and continues training+silymarin (CTS), high intensity interval training (HIT), high intensity interval training+Silymarin (HITS). Silymarin groups, received 300 mg. kg-1.d-1 of silymarin solution through gavage. Animals in HIT groups performed 3-min bouts at 40 m/min, interspersed by 3-min active recovery at a running velocity of 20 m/min on a motorized treadmill with 15% incline, repeated six times per session. Continues training groups performed steady state running at the same speed as the active recovery's speed in the HIT group. Liver histological modifications and serum levels of alanine aminotransferase (ALT) and Aspartate transaminase (AST) were measured. Results: Silymarin consumption and aerobic training were able to improve histological changes compared with control group. Interactive effect of silymarin supplementation and training on AST and ALT levels was not significant. Silymarin reduced liver AST and ALT levels (p≤0.05). Also, AST levels were significantly higher in HIT group than in control group (p≤0.05). The amount of this enzyme in the HITS was significantly reduced compared to HIT group (p≤0.05). Conclusion: Silymarin supplementation and aerobic training separately and in combination may improve liver histological status of rats with dexamethasone-induced nonalcoholic fatty liver.
Exercise Physiology
Hannaneh khalili ateni; Rozita Fathi; khadijeh Nasiri; Abolfazl Akbari
Abstract
Aim: The aim of present study is to evaluate the effects of ten weeks of aerobic exercise and consumption of safflower seed extract on PIK3R1gene expression and serum creatinine levels in male rats, after consuming Dexamethasone.Method: 25 male Wistar rats (371± 32 gr) were randomly divided into ...
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Aim: The aim of present study is to evaluate the effects of ten weeks of aerobic exercise and consumption of safflower seed extract on PIK3R1gene expression and serum creatinine levels in male rats, after consuming Dexamethasone.Method: 25 male Wistar rats (371± 32 gr) were randomly divided into five groups including; control, dexamethasone, dexamethasone + safflower (500 mg/kg of body weight), dexamethasone + aerobic exercise (60 minutes, speed of 28m/min, 5 days a week), dexamethasone + safflower + aerobic exercise. Kidney damage was induced by subcutaneous injection of Dexamethasone (8 gr /kg of body weight) for 6 days. Results: Findings didn’t show a significant effect in the expression of PIK3R1 gene in different groups. Despite the observed changes in renal histology, dexamethasone caused insignificant changes in urea and uric acid. The results of this study showed that 10 weeks of consumption of safflower extract caused a significant decrease in urea and an insignificant increase in uric acid in mice with kidney damage. Also, 10 weeks of aerobic exercise significantly reduced urea, while causing an insignificant reduction in uric acid in mice with kidney damage. Despite changes in urea and uric acid, aerobic exercise and safflower extract can improve kidney damage.Conclusion: It seems that 10 weeks of aerobic exercise and consumption of safflower seed extract can be effective in improving kidney injury but the interveners in this study could not alter the expression of the PIK3R1 gene.
