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首页> 外文期刊>Journal of biochemical and molecular toxicology >Protective effect of hydroxytyrosol in arsenic‐induced mitochondrial dysfunction in rat brain
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Protective effect of hydroxytyrosol in arsenic‐induced mitochondrial dysfunction in rat brain

机译:羟基羟氢溶胶在大鼠脑诱导的线粒体功能障碍中的保护作用

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Abstract The present study was planned to investigate the protective effect of hydroxytyrosol (HT) against arsenic (As)‐induced mitochondrial dysfunction in rat brain. Rats exposed to sodium arsenite (25?ppm for 8 weeks) showed decreased mitochondrial complexes (I, II, IV) activities, mitochondrial superoxide dismutase (MnSOD), and catalase activities in brain mitochondria. As‐treated rats showed reduced mRNA expression of complex I (ND‐1, ND‐2), IV (COX‐1, COX‐4) subunits, and uncoupling protein‐2 (UCP‐2). In addition to this, As exposure downregulated the protein expression of MnSOD. Administration of HT with As restored the enzymatic activities of mitochondrial complexes, MnSOD and catalase, increased the mRNA levels of complexes subunits and UCP‐2 as well as proteins level of MnSOD. These results suggest that HT efficiently restores mitochondrial dysfunction in As neurotoxicity and might be used as potential mitoprotective agent in future.
机译:摘要计划探讨羟基吡咯醇(HT)对大鼠脑中的砷(AS)诱导的线粒体功能障碍的保护作用。 暴露于砷酸钠(25℃持续8周)的大鼠表现出降低的线粒体复合物(I,II,IV)活性,线粒体超氧化物歧化酶(MNSOD)和脑线粒体中的过氧化氢酶活性。 如处理的大鼠显示复合I(ND-1,ND-2),IV(COX-1,COX-4)亚基的MRNA表达,并且解偶联蛋白-2(UCP-2)的mRNA表达。 除此之外,由于曝光下调了MNSOD的蛋白质表达。 HT与恢复线粒体复合物,MNSOD和过氧化氢酶的酶活性的HT,增加了复合物亚基和UCP-2的mRNA水平以及MNSOD的蛋白质水平。 这些结果表明,HT有效地将线粒体功能障碍有效地恢复为神经毒性,并且可以将来用作潜在的隔离剂。

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