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目的研究二氢杨梅素对小鼠的抗疲劳作用,初步探讨其抗疲劳机制。方法将40只雄性小鼠随机分为空白对照组、二氢杨梅素剂量组(40、20、10 mg·kg~(-1)),持续灌胃给药28 d后,通过对小鼠负重游泳实验,记录小鼠负重游泳时间。第29天不负重游泳90 min,分别测定小鼠肝糖原、血乳酸(BLA)、血尿素氮(BUN)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)等生化指标,实时荧光定量逆转录-聚合酶链反应(RT-PCR)法检测过氧化物酶体增殖物激活受体共激活因子-1(PGC-1α)、过氧化物酶体增殖物激活受体α(PPARα)的基因表达。结果与空白对照组相比,二氢杨梅素能够延长小鼠负重游泳时间,增加肝糖原在体内的储备,降低BLA、BUN、MDA水平,提高SOD和GSH-Px活性。实时荧光定量RTPCR结果显示,二氢杨梅素剂量组疲劳小鼠骨骼肌中PGC-1α、PPARα的mRNA表达水平显著升高,且均具有统计学意义。结论二氢杨梅素通过加速自由基的清除,增强小鼠的抗氧化能力,提高小鼠的运动能力发挥抗疲劳作用,其作用亦与骨骼肌中PGC-1α、PPARα基因表达有关联。
Objective To study the anti-fatigue effect of dihydromyricetin on mice, and to explore its anti-fatigue mechanism. Methods Forty male mice were randomly divided into blank control group, dihydromyricetin dose group (40, 20, and 10 mg · kg -1) Swimming experiment, record the mouse weight swimming time. On the 29th day, we did not take any weight-bearing swimming for 90 min. The levels of hepatic glycogen, BLA, BUN, SOD, GSH- (Px), malondialdehyde (MDA) and other biochemical indicators were determined by enzyme-linked immunosorbent assay (ELISA). Peroxisome proliferator activated receptor coactivator-1 (PGC-1α) , Peroxisome proliferator activated receptor α (PPARα) gene expression. Results Compared with the blank control group, dihydromyricetin prolonged the weight-bearing swimming time, increased the glycogen storage in the body, decreased the levels of BLA, BUN and MDA, and increased the activity of SOD and GSH-Px. Real-time fluorescent quantitative RT-PCR results showed that the mRNA expression of PGC-1α and PPARα in the skeletal muscle of dihydromyricetin-treated mice significantly increased, both of which were statistically significant. Conclusions Dihydromyricetin accelerates the free radical scavenging, enhances the anti-oxidation ability of mice, enhances the motor ability of mice and exerts the anti-fatigue effect, and its function is also associated with the expression of PGC-1α and PPARα in skeletal muscle.