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丹参酮 IIA 和隐丹参酮可预防缺氧诱导的 H9c2 细胞线粒体功能障碍:与线粒体 ROS、细胞内一氧化氮和钙水平有关。

Tanshinone IIA and Cryptotanshinone Prevent Mitochondrial Dysfunction in Hypoxia-Induced H9c2 Cells: Association to Mitochondrial ROS, Intracellular Nitric Oxide, and Calcium Levels.

机构信息

Traditional & Complementary Medicine Program, RMIT Health Innovations Research Institute, School of Health Sciences, RMIT University, Bundoora, VIC 3083, Australia.

出版信息

Evid Based Complement Alternat Med. 2013;2013:610694. doi: 10.1155/2013/610694. Epub 2013 Mar 4.

DOI:10.1155/2013/610694
PMID:23533503
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3603679/
Abstract

The protective actions of tanshinones on hypoxia-induced cell damages have been reported, although the mechanisms have not been fully elucidated. Given the importance of nitric oxide (NO) and reactive oxygen species (ROS) in regulation of cell functions, the present study investigated the effects of two major tanshinones, Tanshinone IIA (TIIA) and cryptotanshinone (CT), on hypoxia-induced myocardial cell injury and its relationships with intracellular NO and ROS, calcium, and ATP levels in H9c2 cells. Chronic hypoxia significantly reduced cell viability which accompanied with LDH release, increase in mitochondrial ROS, intracellular NO and calcium levels, decrease in superoxide dismutase (SOD) activity, and cellular ATP contents. TIIA and CT significantly prevented cell injury by increasing cell viability and decreasing LDH release. The protective effects of tanshinones were associated with reduced mitochondrial superoxide production and enhanced mitochondrial SOD activity. Tanshinones significantly reduced intracellular NO and Ca(2+) levels. ATP levels were also restored by TIIA. These findings suggest that the cytoprotective actions of tanshinones may involve regulation of intracellular NO, Ca(2+), ATP productions, mitochondrial superoxide production, and SOD activity, which contribute to their actions against hypoxia injuries.

摘要

丹参酮对缺氧诱导的细胞损伤具有保护作用,其机制虽尚未完全阐明。鉴于一氧化氮(NO)和活性氧(ROS)在调节细胞功能方面的重要性,本研究探讨了两种主要的丹参酮,丹参酮 IIA(TIIA)和隐丹参酮(CT)对 H9c2 细胞缺氧诱导的心肌细胞损伤及其与细胞内 NO 和 ROS、钙和 ATP 水平的关系。慢性缺氧显著降低细胞活力,伴随乳酸脱氢酶(LDH)释放增加、线粒体 ROS、细胞内 NO 和钙水平增加、超氧化物歧化酶(SOD)活性降低以及细胞内 ATP 含量减少。TIIA 和 CT 通过增加细胞活力和减少 LDH 释放显著预防细胞损伤。丹参酮的保护作用与减少线粒体超氧化物生成和增强线粒体 SOD 活性有关。丹参酮还显著降低细胞内 NO 和 Ca2+水平。TIIA 还恢复了 ATP 水平。这些发现表明,丹参酮的细胞保护作用可能涉及调节细胞内 NO、Ca2+、ATP 的产生、线粒体超氧化物的产生和 SOD 活性,这有助于其对抗缺氧损伤的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4583/3603679/ff8b89372188/ECAM2013-610694.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4583/3603679/ff8b89372188/ECAM2013-610694.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4583/3603679/ff8b89372188/ECAM2013-610694.002.jpg

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