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

机译:当归当归对血管紧张素Ⅱ诱导的H9c2心肌细胞凋亡的保护作用

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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.
机译:背景当归(当归)是一种常用于中药的草药。它用于促进血液流动,并已用于治疗动物模型中的心肌缺血/再灌注损伤。血管紧张素II(Ang II)已显示在介导心血管疾病中起重要作用,并可能导致心脏肥大和细胞凋亡。本研究旨在探讨当归是否对Ang II诱导的H9c2心肌细胞凋亡具有保护作用,并研究其机制。方法我们在体外模型中评估了当归对Ang II诱导的细胞凋亡的影响。 H9c2心肌母细胞在无血清培养基中培养4小时,然后在Ang II处理之前或之后用当归(50,100?μg/ ml)1小时处理。再培养23小时后,收集细胞进行凋亡标记物和细胞信号通路测定分析。结果我们的结果表明,Ang II诱导凋亡前坏死的上调,线粒体膜电位的不稳定性,细胞色素c的释放,caspase-9和caspase-3的活化以及心肌细胞的凋亡。当归的预处理或后处理可逆转上述所有Ang II诱导的H9c2细胞凋亡作用。此外,JNK(SP600125)抑制剂完全阻断了当归在Ang II处理的H9c2细胞中对caspase-3活化的抑制作用。结论我们的结果表明当归在治疗前或治疗后均可大大减轻Ang II诱导的心肌细胞凋亡。这些发现表明当归的抗凋亡作用是由JNK和PI3k抑制剂介导的。

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