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首页> 外文期刊>Reproduction, fertility, and development >Carnitine-mediated antioxidant enzyme activity and Bcl2 expression involves peroxisome proliferator-activated receptor-gamma coactivator-1 alpha in mouse testis
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Carnitine-mediated antioxidant enzyme activity and Bcl2 expression involves peroxisome proliferator-activated receptor-gamma coactivator-1 alpha in mouse testis

机译:肉碱介导的抗氧化酶活性和BCl2表达涉及过氧酶体增殖物 - 活化的受体-γ-1α在小鼠睾丸中

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The protective effects of carnitine have been attributed to inhibition of apoptosis, alleviating oxidative stress and DNA repair mechanism by decreasing oxidative radicles. Carnitine also increases mitochondrial biogenesis via peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1 alpha). The role of carnitine in testicular PGC1 alpha expression has not been documented. We hypothesised that the effects of carnitine as an antioxidant, inhibitor of apoptosis and controller of steroidogenesis in mouse testis may involve PGC1 alpha as a regulator. The present study was designed to evaluate the localisation of PGC1 alpha and the effects of carnitine treatment on the expression of PGC1 alpha, Bcl2 and antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)) in mouse testis and serum testosterone concentrations. PGC1 alpha was primarily immunolocalised to the Leydig cells and primary spermatocytes. Western blot analysis showed that carnitine (50mgkg(-1) and 100mgkg(-1) for 7 days) significantly increased PGC1 alpha and Bcl2 expression in the testis in a dose-dependent manner. In addition, carnitine treatment significantly increased antioxidant enzyme (CAT, SOD and GPx) levels. The carnitine-induced changes in PGC1 alpha in the testis were significantly correlated with changes in serum testosterone concentrations, as well as with changes in Bcl2 expression and antioxidant enzyme activity in the testis, as evaluated by electrophoresis. Therefore, the results of the present study suggest that carnitine treatment of mice increases PGC1 alpha levels in the testis, which may, in turn, regulate steroidogenesis by increasing expression of Bcl2 and antioxidant enzymes.
机译:肉碱的保护作用归因于凋亡的抑制,通过降低氧化碱来减轻氧化应激和DNA修复机制。肉毒碱还通过过氧化物体增殖物激活的受体-γ-1α(PGC1α)增加线粒体生物。肉碱在睾丸中的作用尚未记录睾丸PGC1α表达。我们假设肉碱作为抗氧化剂的影响,小鼠睾丸中凋亡凋亡抑制剂和甾体系控制器的抑制剂可能涉及PGC1α作为调节剂。本研究旨在评估PGC1α的定位和肉碱治疗对小鼠睾丸(超氧化物歧化酶),过氧化物(SOD),过氧化物(GPX)的抗氧化酶(超氧化物歧化酶(SOD),过氧化物过氧化物酶(GPX)的影响和血清睾酮浓度。 PGC1α主要免疫胶质化到Leydig细胞和原发性精子胶质细胞。 Western印迹分析表明,肉碱(50mgkg(-1)和100mgkg(-1)7天,以剂量依赖性方式显着增加了睾丸中的PGC1α和BCL2表达。此外,肉碱治疗显着增加抗氧化酶(猫,SOD和GPX)水平。与睾丸睾酮浓度的变化以及通过电泳评估的睾丸睾酮浓度的变化以及睾丸中的Bcl2表达和抗氧化酶活性的变化显着相关。因此,本研究的结果表明小鼠的肉碱治疗增加了睾丸中的PGC1α水平,其可以通过增加BCl2和抗氧化酶的表达来调节甾体制度。

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