Angiotensin II (Ang II) is an important bioactive peptide in the renin‑angiotensin system, and it can contribute to cell proliferation and cardiac hypertrophy. Dysfunctions in transient receptor potential canonical (TRPC) channels are involved in many types of cardiovascular diseases. The aim of the present study was to investigate the role of the TRPC channel inhibitor SKF‑96365 in cardiomyocyte hypertrophy induced by Ang II and the potential mechanisms of SKF‑96365. H9c2 cells were treated with different concentrations of Ang II. The expression levels of cardiomyocyte hypertrophy markers and TRPC channel‑related proteins were also determined. The morphology and surface area of the H9c2 cells, the expression of hypertrophic markers and TRPC channel‑related proteins and the [3H] leucine incorporation rate were detected in the Ang II‑treated H9c2 cells following treatment with the TRPC channel inhibitor SKF‑96365. The intracellular Ca2+ concentration was tested by flow cytometry. The present results suggested that the surface area of H9c2 cells treated with Ang II was significantly increased compared with untreated H9c2 cells. The fluorescence intensity of α‑actinin, the expression of hypertrophic markers and TRPC‑related proteins, the [3H] leucine incorporation rate and the intracellular Ca2+ concentration were all markedly increased in the Ang II‑treated H9c2 cells but decreased following SKF‑96365 treatment. The present results suggested that Ang II induced cardiomyocyte hypertrophy in H9c2 cells and that the TRPC pathway may be involved in this process. Therefore, SKF‑96365 can inhibit cardiomyocyte hypertrophy induced by Ang II by suppressing the TRPC pathway. The present results indicated that TRPC may be a therapeutic target for the development of novel drugs to treat cardiac hypertrophy.

译文

血管紧张素II(Ang II)是肾素-血管紧张素系统中的重要生物活性肽,可促进细胞增殖和心脏肥大。瞬态受体电位经典(TRPC)通道功能异常涉及多种类型的心血管疾病。本研究的目的是研究TRPC通道抑制剂SKF‑96365在AngⅡ诱导的心肌肥大中的作用以及SKF‑96365的潜在机制。用不同浓度的Ang II处理H9c2细胞。还确定了心肌肥大标志物和TRPC通道相关蛋白的表达水平。经TRPC通道抑制剂SKF‑96365处理后,在经Ang II处理的H9c2细胞中检测到H9c2细胞的形态和表面积,肥厚标记和TRPC通道相关蛋白的表达以及[3H]亮氨酸掺入率。通过流式细胞仪测试细胞内Ca 2浓度。本结果表明,与未处理的H9c2细胞相比,用AngⅡ处理的H9c2细胞的表面积显着增加。 Ang II处理的H9c2细胞中α-肌动蛋白的荧光强度,肥大标记和TRPC相关蛋白的表达,[3H]亮氨酸掺入率和细胞内Ca2浓度均显着增加,但经SKF‑96365处理后降低。目前的结果表明Ang II诱导了H9c2细胞中的心肌肥大,并且TRPC途径可能参与了这一过程。因此,SKF‑96365可通过抑制TRPC途径来抑制AngⅡ诱导的心肌肥大。本结果表明,TRPC可能是开发用于治疗心脏肥大的新药的治疗靶标。

+1
+2
100研值 100研值 ¥99课程
检索文献一次
下载文献一次

去下载>

成功解锁2个技能,为你点赞

《SCI写作十大必备语法》
解决你的SCI语法难题!

技能熟练度+1

视频课《玩转文献检索》
让你成为检索达人!

恭喜完成新手挑战

手机微信扫一扫,添加好友领取

免费领《Endnote文献管理工具+教程》

微信扫码, 免费领取

手机登录

获取验证码
登录