血管紧张素转换酶抑制肽LAP活性对血管平滑肌凋亡的分子机制研究

Yi Shen, Hong Fang, A. O. Cavdar, Chi Liu
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引用次数: 0

摘要

通过观察自发性高血压大鼠腹主动脉凋亡细胞、Bcl-2/Bax和caspase-9的表达水平,探讨血管紧张素转换酶抑制肽LAP对血管平滑肌细胞凋亡的影响及其机制。选取20只雄性SHRs,检测凋亡细胞及凋亡相关蛋白(Bcl-2、Bax、caspase-9)的表达情况。LAP组细胞凋亡指数明显低于对照组。LAP组Bcl-2表达明显高于对照组。而LAP组Bax和caspase-9的表达水平明显低于对照组。凋亡指数与Bcl-2呈负相关,与Bax/caspase-9呈正相关。同样,LAP组的炎症指标明显低于对照组。经LAP处理后,腹腔动脉中Angⅱ的表达明显降低。血管紧张素转换酶抑制肽LAP通过上调SHRs中Bcl-2、下调Bax和caspase-9抑制血管平滑肌细胞凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Molecular Mechanisms of Angiotensin-converting Enzyme Inhibitory Peptide LAP Activity on Apoptosis of Vascular Smooth Muscle
We observe the expression levels of apoptotic cells, Bcl-2/Bax and caspase-9 on abdominal aorta of spontaneously hypertensive rats (SHRs) to investigate impact and mechanisms of angiotensin converting enzyme inhibitory peptide LAP in apoptosis of vascular smooth muscle cell. A total of 20 male SHRs were studied to detect apoptotic cells and the expression of apoptosis-related proteins (Bcl-2, Bax, caspase-9). The index of apoptotic cells in LAP group was significantly lower compared to the control group. The expression of Bcl-2 in the LAP group was significantly higher than the control group. However, the levels of Bax and caspase-9 expression in the LAP group were significantly lower compared to the control group. The apoptosis index was negatively correlated with Bcl-2 and positively correlated with Bax/caspase-9. Similarly, the inflammation markers in LAP group were significantly lower than those in the control group. The expression of Ang II was significantly decreased after treating with LAP in the abdominal arteries. Angiotensin- converting- enzyme inhibition peptide LAP inhibited apoptosis of vascular smooth muscle cells through up-regulation of Bcl-2 and down-regulation of Bax and caspase-9 in SHRs.
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