Tanshinone IIA protects neonatal rat cardiomyocytes from adriamycin-induced apoptosis
Tanshinone IIA protects neonatal rat cardiomyocytes from adriamycin-induced apoptosis
复制标题
丹参酮 IIA 保护新生大鼠心肌细胞免受阿霉素诱导的细胞凋亡
DOI：
10.1016/j.trs1.2007.11.005
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发表时间：
2008-02-01
影响因子：
7.8
通讯作者：
Liu, Peiqing
中科院分区：
文献类型：
--
作者：
Gao, Jie;Yang, Guoqing;Liu, Peiqing
丹参酮IIA （TSN）是从中药丹参中提取的单体。在这项研究中，我们研究了丹参酮IIA对阿霉素（ADR）诱导的新生大鼠心肌细胞凋亡的影响及其分子机制。原代培养的心肌细胞分别用1 μ mol/L阿霉素处理24 h，丹参酮IIA （0.5-2 μ mol/L）预处理2 h，采用3-（4,5-二甲基噻唑-2基）-2,5-二苯基溴化四唑（MTT）法、Hoechst染色法和流式细胞术检测细胞活力和凋亡情况。用荧光探针2′，7′-二氯荧光素双乙酸酯和二氢乙啶检测活性氧的产生。Western blotting检测Bcl-2和Bax蛋白的表达。阿霉素显著诱导心肌细胞凋亡。丹参酮IIA （0.5 ~ 2 μ mol/L）对阿霉素诱导的细胞凋亡有改善作用，且呈剂量依赖性。丹参酮IIA （2 μ mol/L）显著减弱阿霉素诱导的活性氧生成。Western blotting结果显示，丹参酮IIA可阻止阿霉素介导的Bcl-2/Bax比值的降低。综上所述，丹参酮IIA显著抑制阿霉素诱导的心肌细胞凋亡，并呈剂量依赖性，这种作用至少部分是由其抗氧化特性引起的。
Tanshinone IIA (TSN) is a monomer extracted from the Chinese herb Danshen. In this study, we examined the effect of Tanshinone IIA on adriamycin (ADR)-induced apoptosis in neonatal rat cardiomyocytes and underlying molecular mechanisms. Primary cultured cardiomyocytes were treated with 1 mu mol/L of adriamycin for 24 h with or without pretreatment with Tanshinone IIA (0.5-2 mu mol/L) for 2 h. 3-(4,5-dimethyl thiazol-2yl)-2,5-diphenyltetrazolium bromide (MTT) assay, Hoechst staining, and flow cytometry measurement were used to assess cell viability and apoptosis. Fluorescent probes 2',7'-dichlorofluorescein diacetate and dihydroethidium were used to detect the production of reactive oxygen species. Western blotting was used to evaluate the expression of Bcl-2 and Bax proteins. Adriamycin significantly induced apoptosis in cardiomyocytes. Tanshinone IIA (0.5-2 mu mol/L) ameliorated apoptosis induced by adriamycin in a dose-dependent manner. Tanshinone IIA (2 mu mol/L) markedly attenuated adriamycin-induced reactive oxygen species production. Western blotting revealed that Tanshinone IIA prevented the adriamycin-mediated reduction of the ratio of Bcl-2/Bax. In conclusion, Tanshinone IIA significantly inhibits adriamycin-induced cardiomyocyte apoptosis in a dose-dependent manner, and this effect is at least partly caused by its antioxidant properties.