运动对肥胖大鼠心脏组织FoxO1表达影响的比较

Farzad Zandian, Hosein Sazegar
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摘要

背景与目的:FoxO1基因是心脏组织细胞代谢的重要调控因子。因此,本研究的目的是探讨克氏花提取物和运动对大鼠维管组织FoxO1基因表达的影响。材料与方法:选取体重180 ~ 200 g的成年雄性Wistar大鼠30只,分为5组:对照组、阴性对照组、1组运动肥胖大鼠和400、800 mg / Kg克氏花提取物治疗组。采用Real Time RT - PCR对30只大鼠心脏进行分子检测。最后采用SPSS软件进行表达检验,并进行ANOVA test和LSD检验,显著性水平P <0.05。结果:与肥胖组相比,400 mg / kg剂量的雪蚤提取物可显著降低FoxO1基因表达(0.61±0.14 ab),而800剂量的雪蚤提取物(0.70±0.25 ab)可显著降低FoxO1基因表达(0.61±0.14 ab)。差异有统计学意义(p <0.05)。此外,在运动组中,与肥胖组相比,我们的基因表达减少(0.54±0.13 b)。另一方面,生化测试结果证实,400 mg / kg的Kelussia处理大鼠的肥胖大鼠心脏因子减少。讨论与结论:运动和克鲁索提取物可以降低FoxO1基因的表达,如果在未来的研究中得到证实,可能是心脏病的治疗靶点。
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Comparison of the effect of exercise with Kelussia Odaratissma Mozaff on FoxO1 Expression level in cardiac tissue of obese rats
Background and Aim: The FoxO1 gene is an important regulator of cellular metabolism in heart tissue. Therefore, the aim of this study was to investigate the effect of Kelussia extract and exercise on FoxO1 gene expression in vascular tissue. Materials & Methods: In the present study, 30 adult male Wistar rats weighing 180 to 200 g were selected and divided into five groups of control, negative control, one group of obese rats with exercise and two treatment groups with doses of 400 and 800 mg / Kg of Kelussia extract were divided. Molecular tests were performed on the hearts of 30 rats using Real Time RT PCR. Finally, expression test was performed using SPSS software and ANOVA TEST and LSD tests with a significance level of P <0.05. Results: Kelussia extract at a dose of 400 mg / kg can significantly reduce the expression of FoxO1 gene (0.61 ± 0.14 ab) compared to the 800 dose (0.70 ± 0.25 ab) compared to the obese group. Statistically significant was significant (p <0.05). Also, in the group of rats with exercise, we had a decrease in gene expression compared to the obese group (0.54 ± 0.13 b). On the other hand, the results of biochemical tests confirmed the reduction of factors in the hearts of obese rats in rats treated with 400 mg / kg of Kelussia. Discussion and Conclusion: Exercise as well as Kelussia extract can reduce the expression of the FoxO1 gene and, if confirmed in future studies, could be a therapeutic target in heart disease.
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