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首页> 外文期刊>Journal of cellular biochemistry. >Protective effects of cynaroside against HO-induced apoptosis in H9c2 cardiomyoblasts.
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Protective effects of cynaroside against HO-induced apoptosis in H9c2 cardiomyoblasts.

机译：芥子苷对H9c2心肌细胞中HO诱导的细胞凋亡的保护作用。

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Flavonoids with potent anti-oxidative effects are the major effective components in traditional herbal medicine used in treating cardiovascular diseases. Cynaroside is a flavonoid compound that exhibits anti-oxidative capabilities. However, little is known about its effect on oxidative injury to cardiac myocytes and the underlying mechanisms. This study was designed to investigate the protective effects of cynaroside against H(2) O(2) -induced apoptosis in H9c2 cardiomyoblasts. H9c2 cells were pretreated with cynaroside for 4 h before exposure to 150 microM H(2) O(2) for 6 h. H(2) O(2) treatment caused severe injury to the H9c2 cells, which was accompanied by apoptosis, as revealed by analysis of cell nuclear morphology, through Annexin V FITC/PI staining and caspase proteases activation. Cynaroside pretreatment significantly reduced the apoptotic rate by enhancing the endogenous anti-oxidative activity of superoxide dismutase, glutathione peroxidase, and catalase, thereby inhibiting intracellular reactive oxygen species (ROS) generation. Moreover, cynaroside moderated H(2) O(2) -induced disruption of mitochondrial membrane potential, increased the expression of anti-apoptotic protein Bcl-2 while decreased the expression of pro-apoptotic protein Bax, and thereby inhibited the release of apoptogenic factors (cytochrome c and smac/Diablo) from mitochondria in H9c2 cells. Our data also demonstrated that cynaroside pretreatment showed an inhibitory effect on the H(2) O(2) -induced increase in c-Jun N-terminal kinase (JNK) and P53 protein expression. These results suggest that cynaroside prevents H(2) O(2) -induced apoptosis in H9c2 cell by reducing the endogenous production of ROS, maintaining mitochondrial function, and modulating the JNK and P53 pathways.
机译：具有有效抗氧化作用的类黄酮是用于治疗心血管疾病的传统草药的主要有效成分。 Cynaroside是一种类黄酮化合物，具有抗氧化能力。然而，关于其对心肌细胞氧化损伤及其潜在机制的影响知之甚少。这项研究旨在调查对H9c2心肌母细胞中H（2）O（2）诱导的细胞凋亡的cynaroside的保护作用。 H9c2细胞用cynaroside预处理4 h，然后再暴露于150 microM H（2）O（2）6 h。 H（2）O（2）治疗对H9c2细胞造成了严重伤害，并伴随着细胞凋亡，正如通过膜联蛋白V FITC / PI染色和胱天蛋白酶蛋白酶活化所显示的细胞核形态分析所揭示的那样。 Cynaroside预处理通过增强超氧化物歧化酶，谷胱甘肽过氧化物酶和过氧化氢酶的内源性抗氧化活性，从而显着降低了细胞凋亡率，从而抑制了细胞内活性氧（ROS）的产生。此外，cynaroside调节了H（2）O（2）诱导的线粒体膜电位破坏，增加了抗凋亡蛋白Bcl-2的表达，同时降低了促凋亡蛋白Bax的表达，从而抑制了凋亡因子的释放。 H9c2细胞中的线粒体（细胞色素c和smac / Diablo）。我们的数据还表明，cynaroside预处理对H（2）O（2）诱导的c-Jun N末端激酶（JNK）和P53蛋白表达增加具有抑制作用。这些结果表明，通过减少内源性ROS，维持线粒体功能以及调节JNK和P53途径，西拉糖苷可防止H（2）O（2）诱导H9c2细胞凋亡。

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