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目的研究观察游泳训练,补充α-硫辛酸以及联合干预方式(游泳+α-硫辛酸)对Ⅱ型糖尿病大鼠心肌组织氧化应激指标、抗氧化酶及线粒体生物合成的影响,并初步探讨其内在作用机制。方法 60只Wistar大鼠在完成Ⅱ型糖尿病造模后,随机分成4组,即糖尿病对照组(CON)、α-硫辛酸(LA)组、游泳训练组(ST)和α-硫辛酸+游泳训练组(ST+LA)。ST组和ST+LA组进行游泳训练。训练方案为:60 min/d,周一至周五训练,共计8周。试剂盒测定大鼠心肌组织丙二醛(MDA)及过氧化脂(LPO)水平;Western blot方法检测线粒体抗氧化酶系MnSOD,Thi-ored-2,Prdx3,线粒体合成调节因子PGC-1α及二相酶HO-1,γ-GCL,NQO-1表达水平;透射电镜观察线粒体生物合成变化。结果 LA和ST均可显著性降低心肌组织中MDA含量,且联合作用效果存在放大效应(P<0.05);LPO的变化趋势与MDA相似。对于抗氧化酶的影响,ST既可有效提高线粒体抗氧化酶活性,又可显著性提高胞浆解毒酶蛋白表达(P<0.05);LA,除了显著性提高HO-1,γ-GCL外,对NQO-1及线粒体抗氧化酶的影响不具有统计学意义(P>0.05)。另外,ST和LA均可使线粒体数目增加,且在联合干预后,增强作用实现了优势互补(P<0.05)。结论联合作用方式引起的心肌保护作用与其提高抗氧化酶(实现单一干预方式对胞浆中抗氧化酶提高的叠加效应)相关。另外,联合作用在增加线粒体生物合成水平上存在优势增强效应。
Objective To investigate the effects of swimming training, α-lipoic acid supplementation and combined intervention (swimming + α-lipoic acid) on oxidative stress, antioxidase and mitochondrial biosynthesis in myocardium of type 2 diabetic rats. Internal mechanism of action. Methods Sixty Wistar rats were randomly divided into 4 groups: diabetic control group (CON), α-lipoic acid (LA) group, swimming training group (ST) and α-lipoic acid + swimming Training group (ST + LA). ST group and ST + LA group for swimming training. Training program: 60 min / d, Monday to Friday training, a total of 8 weeks. The contents of malondialdehyde (MDA) and lipid peroxidation (LPO) in myocardial tissue of rats were determined by kit. The mitochondrial antioxidant enzymes such as MnSOD, Thi-ored-2, Prdx3, mitochondrial synthesis regulator PGC- The expression of HO-1, γ-GCL and NQO-1 were detected by transmission electron microscopy. The changes of mitochondrial biosynthesis were observed by transmission electron microscopy. Results Both LA and ST significantly decreased the content of MDA in myocardial tissue, and the synergistic effects were magnified (P <0.05). The change trend of LPO was similar to that of MDA. For antioxidant enzymes, ST could not only increase mitochondrial antioxidant enzyme activity but also significantly increase cytoplasmic detoxification enzyme protein expression (P <0.05). In addition to the significant increase of HO-1 and γ-GCL, The effect on NQO-1 and mitochondrial antioxidant enzymes was not statistically significant (P> 0.05). In addition, both ST and LA could increase the number of mitochondria, and after the combination intervention, the enhancement effect achieved the complementary advantages (P <0.05). Conclusions The myocardial protective effect induced by the combined action is related to the enhancement of anti-oxidase (the superposition effect of single intervention on anti-oxidase in the cytoplasm). In addition, the combined effect of increasing mitochondrial bio-synthesis level there is an advantage to enhance the effect.