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Alteration of mitochondrial function and ultrastructure in the hippocampus of pilocarpine-treated rat

机译:毛果芸香碱处理的大鼠海马线粒体功能和超微结构的变化

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Present studies were carried out to decipher seizure-dependent changes in mitochondrial function and ultrastructure in rat hippocampus after status epilepticus (SE) induced by pilocarpine (PILO). Discernible mitochondrial ultrastructural damage was observed in the hippocampus. Enzyme assay revealed cytochrome oxidase (COX) activity significantly increased 3. h after SE, decreased 7. d and 45. d after SE, whereas succinate dehydrogenase (SDH) activity displayed no significant changes. Quantitative real-time PCR and Western blotting showed that COX III (mitochondrial-encoded) mRNA and protein level were significantly increased at 3. h, decreased to the control level on 7. d and dropped significantly on 45. d; the corresponding expression of COX IV were not changed by PILO at any time tested. The results were also supported by immunohistochemistry. Thus, our results demonstrate that dysfunction of mitochondrial complex IV respiratory enzyme and mitochondrial ultrastructural damage in the hippocampus are associated with prolonged seizure during experimental temporal lobe epilepsy and mitochondria are more vulnerable to epileptic damage.
机译:目前的研究旨在破译毛果芸香碱(PILO)引起的癫痫持续状态(SE)后大鼠海马线粒体功能和超微结构的癫痫发作依赖性变化。在海马中观察到明显的线粒体超微结构损伤。酶法检测表明,SE后3 h细胞色素氧化酶(COX)活性显着升高,SE后分别降低7. d和45 d,而琥珀酸脱氢酶(SDH)活性未见明显变化。实时荧光定量PCR和Western印迹表明,COX III(线粒体编码)的mRNA和蛋白质水平在3. h时显着升高,在7. d时降至对照水平,在45 d时显着下降。在任何时候,PILO都不会改变COX IV的相应表达。免疫组织化学也支持该结果。因此,我们的结果表明,在实验性颞叶癫痫期间,海马线粒体复合物IV呼吸酶功能异常和线粒体超微结构损伤与癫痫发作时间长有关,而线粒体更容易受到癫痫性损伤的影响。

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