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