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Mitochondrial fusion/fission process involved in the improvement of catalpol on high glucose- induced hepatic mitochondrial dysfunction
  • ISSN号:1672-9145
  • 期刊名称:《生物化学与生物物理学报:英文版》
  • 时间:0
  • 分类:Q244[生物学—细胞生物学] O411.1[理学—理论物理;理学—物理]
  • 作者机构:[1]Jiangsu Center of Drug Screening, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing 210009, China, [2]Jiangsu Center for Pharmacodynamics Research and Evaluation, China Pharmaceutical University, Nanjing 210009, China, [3]Qinghai Yangzong Pharmaceutial Co., Ltd, Xining 810003, China, [4]Tianjin Institute of Pharmaceutical Research, Tianjin 300193, China
  • 相关基金:This work was supported by the grants from the National Natural Science Foundation of China (Nos. 81403154 and 81320108029),the National 12th Five-year Plan (No. 2012ZX09504001-001), and the 111 Project (111-2-07).
中文摘要:

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。

英文摘要:

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.

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期刊信息
  • 《生物化学与生物物理学报:英文版》
  • 北大核心期刊(2004版)
  • 主管单位:
  • 主办单位:中国科学院上海生物化学研究所
  • 主编:
  • 地址:上海岳阳路319号
  • 邮编:200031
  • 邮箱:abbs@sibs.ac.cn
  • 电话:021-54920956 54920955
  • 国际标准刊号:ISSN:1672-9145
  • 国内统一刊号:ISSN:31-1940/Q
  • 邮发代号:4-210
  • 获奖情况:
  • 国内外数据库收录:
  • 美国化学文摘(网络版),英国农业与生物科学研究中心文摘,荷兰文摘与引文数据库,美国生物医学检索系统,美国剑桥科学文摘,美国科学引文索引(扩展库),美国生物科学数据库,英国动物学记录,日本日本科学技术振兴机构数据库,中国中国科技核心期刊,中国北大核心期刊(2004版),英国英国皇家化学学会文摘,中国北大核心期刊(2000版)
  • 被引量:5851