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当归(Angelicae Sinensis Radix)对血管紧张素Ⅱ诱导的 H9c2 心肌细胞凋亡的保护作用。

Protective effect of Danggui (Radix Angelicae Sinensis) on angiotensin II-induced apoptosis in H9c2 cardiomyoblast cells.

机构信息

School of Medical Laboratory and Biotechnology, Chung Shan Medical University, No,110, Sec,1, Jianguo N, Rd,, Taichung 40201, Taiwan.

出版信息

BMC Complement Altern Med. 2014 Sep 25;14:358. doi: 10.1186/1472-6882-14-358.

Abstract

BACKGROUND

Danggui (Radix Angelicae Sinensis) is an herb often used in Traditional Chinese medicine. It is used to promote blood flow and has been used in the treatment of myocardial ischemia-reperfusion injury in animal models. Angiotensin II (Ang II) has been shown to play important roles in mediating cardiovascular diseases, and may cause cardiac hypertrophy and apoptosis. This study aimed to investigate whether Danggui has protective effects on Ang II-induced apoptosis in H9c2 cardiomyoblast cells and study the mechanisms involved.

METHODS

We evaluated the effect of Danggui on Ang II-induced apoptosis in an in vitro model. H9c2 cardiomyoblast cells were cultured in serum-free medium for 4 hr, then treated with Danggui (50, 100 μg/ml) 1 hr pre- or post-Ang II treatment. After a further 23 hr of culture, cells were harvested for analyses with assays for apoptosis markers and cell signaling pathways.

RESULTS

Our results showed that Ang II induced upregulation of pro-apoptotic Bad, instability of the mitochondria membrane potential, cytochrome c release, caspase-9 and caspase-3 activation and cardiomyocyte apoptosis. Pre- or post-treatment with Danggui reversed all of the above Ang II-induced apoptotic effects in H9c2 cells. Furthermore, the JNK (SP600125) inhibitor completely blocked Danggui inhibition of caspase-3 activation in Ang II-treated H9c2 cells.

CONCLUSIONS

Our results showed that Danggui either pre-treatment or post-treatment highly attenuated the Ang II-induced apoptosis in cardiomyoblast cells. The findings demonstrated that the anti-apoptosis effect of Danggui is mediated by JNK and PI3k inhibitors.

摘要

背景

当归(当归根)是一种常用于中药的草药。它用于促进血液流动,并已用于动物模型中治疗心肌缺血再灌注损伤。血管紧张素 II(Ang II)已被证明在介导心血管疾病中起重要作用,并且可能导致心肌肥大和细胞凋亡。本研究旨在探讨当归对 Ang II 诱导的 H9c2 心肌细胞凋亡是否具有保护作用,并研究其相关机制。

方法

我们评估了当归对体外模型中 Ang II 诱导的细胞凋亡的影响。将 H9c2 心肌细胞在无血清培养基中培养 4 小时,然后用 Ang II(50、100 μg/ml)预处理或后处理 1 小时。进一步培养 23 小时后,收集细胞进行凋亡标志物和细胞信号通路分析。

结果

我们的结果表明,Ang II 诱导促凋亡 Bad 的上调、线粒体膜电位的不稳定性、细胞色素 c 释放、caspase-9 和 caspase-3 的激活以及心肌细胞凋亡。当归预处理或后处理均可逆转 Ang II 诱导的 H9c2 细胞中的上述所有凋亡作用。此外,JNK(SP600125)抑制剂完全阻断了 Ang II 处理的 H9c2 细胞中当归抑制 caspase-3 激活的作用。

结论

我们的结果表明,当归预处理或后处理均可显著减弱 Ang II 诱导的心肌细胞凋亡。研究结果表明,当归的抗凋亡作用是通过 JNK 和 PI3k 抑制剂介导的。

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