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作 者:曾露露[1] 王佳奇[1] 黄宝亮[1] 陈凯[1] 王月亮 宋明铭 丁传波[1] 郑毅男[1] 徐晓华[2] 刘文丛[1]
机构地区:[1]吉林农业大学中药材学院,长春130118 [2]吉林大学中日联谊医院,长春130051
出 处:《中国药学杂志》2016年第23期2025-2029,共5页Chinese Pharmaceutical Journal
基 金:国家科技部科技型中小企业技术创新基金资助项目(13C26212201221)
摘 要: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 its anti-fatigue mechanism. METH- ODS Forty male mice were randomly divided into blank control group and dihydromyricetin dose groups (40, 20, 10 mg ·kg-1), with continual intragastric administration for 28 d. Through the weight loading swimming experiment of mice, the swimming time of mice were recorded. On the twenty-nine day, mice swam 90 min without loading, and then the activities of BUN, BLA in the serum of mice and biochemical indicators of SOD, GSH-Px, MDA and hepatic glycogen etc were respectively determined. The expression of mR- NA of PGC-1α and PPARα were detected by real-time PCR. RESULTS Comparing with the blank control group, dihydromyricetin dose group can prolong the loaded-swimming time of mice, increase the reserve of liver glycogen in the body, reduce levels of BLA, BUN and MDA, and significantly increased the activities of SOD and GSH-Px. RT-PCR results showed that the expression levels of PGC-1 ct and PPARc~ mRNA in skeletal muscle of mice in the dihydromyricetin dose group were significantly increased, and all had statistical significance. CONCLUSION Dihydromyricetin can accelerate clearance of free radical, enhance mice antioxidant capacity and improve exercise ability in fatigued mice thus play the anti-fatigue role, exercise-induced fatigue is corre- lated with PGC-1α.
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