Catalpol, iridoid glycoside,被显示了由 rescuing mitochondrial 功能,而是详细机制遗体施加血糖过低的效果不清楚还。在这研究,在糖尿病的条件下面的肝的线粒体上的 catalpol 的效果和机制进一步被检验。catalpol 的口头的管理显著地在高脂肪的导致食谱、导致 streptozotocin 的糖尿病的老鼠减少了血葡萄糖, triglyceride,和胆固醇层次。另外, catalpol 在源于糖尿病的肝 mitochondrial ATP 内容稀释了减少。而且,拥有一种长尺寸的线粒体的数字在对待 catalpol 的老鼠被增加。有趣地, mitochondrial 功能的导致 catalpol 的恢复与减少的分裂蛋白质 1 被联系并且 dynamin 相关的蛋白质象增加的 mitofusin 一样的 1 个表达式在肝的 1 个表达式。在 HepG2 房间, catalpol 减轻了 ATP 内容和 mitochondrial 膜潜力的减少,并且反应的氧种类形成的增加由高葡萄糖导致了。当房间与 catalpol 被对待时,线粒体的管状的特征被维持的米托特拉克·格林污点表演。Catalpol 也减少了分裂蛋白质 1 并且 dynamin 相关的蛋白质 1 表情和增加的 mitofusin 在 HepG2 房间的 1 表情。现在的结果建议 catalpol 能改善在一名糖尿病患者下面的肝的 mitochondrial 机能障碍状态,和这可能与它 mitochondrial 的规定有关熔化和分裂事件。
Catalpol, an iridoid glycoside, has been shown to exert hypoglycemic effect by rescuing mitochon- drial function, but the detailed mechanism remains unclear yet. In this study, the effect and mechan- ism of catalpol on the hepatic mitochondria under diabetic conditions were further examined. Oral administration of catalpol significantly reduced the blood glucose, triglyceride, and cholesterol levels in high-fat diet- and streptozotocin-induced diabetic mice. Additionally, catalpol attenuated the decrease in liver mitochondrial ATP content resulting from diabetes. Furthermore, the number of mitochondria possessing a long size was increased in catalpol-treated mice. Interestingly, the catal- pol-induced recovery of mitochondrial function was associated with decreased fission protein 1 and dynamin-related protein 1 expression as well as increased mitofusin 1 expression in the liver. In HepG2 cells, catalpol alleviated the decrease of ATP content and mitochondrial membrane potential, and the increase of reactive oxygen species formation induced by high glucose. MitoTracker Green stain shows that the tubular feature of mitochondria was maintained when cells were treated with catalpol. Catalpol also decreased fission protein 1 and dynamin-related protein 1 expression and in- creased mitofusin 1 expression in HepG2 cells. The present results suggest that catalpol can ameli- orate hepatic mitochondrial dysfunction under a diabetic state, and this may be related to its regulation of mitochondrial fusion and fission events.