Title: Role of PI3K/AKt/e NOS signal pathway in course of H2S inhibiting myocardial hypertrophy induced by ET-1
Abstract: Objective To observe the role of PI3K/AKt/e NOS signal pathway in course of H2 S inhibiting myocardial hypertrophy induced by endothelin-1(ET-1). Methods The neonatal myocardial cells were cultured in vitro and randomly divided into 6 groups including 1control group treated with serum-free DMEM medium, 2hypertrophy group, with 10-8 mol/l ET-1, 310-15 M Na HS group, with 10-15 mol/l Na HS+10-8 mol/l ET-1, 410-14 M Na HS group, with 10-14 mol/l Na HS+10-8 mol/l ET-1, 510-13 M Na HS group, with 10-13 mol/l Na HS+10-8 mol/l ET-1, and 610-12 M Na HS group, with 10-12 mol/l Na HS+10-8 mol/l ET-1. After 24 h, cell surface area and total protein content of myocardial cells and nitric oxide(NO) content in nutrient solution were detected in all groups. The m RNA levels of atrial natriuretic peptide(ANP), B-type natriuretic peptide(BNP), phosphatidylinositol-3-kinase(PI3K), protein kinase B(PKB/AKt) and endothelial nitric oxide synthase(e NOS) were detected by using RT-PCR. The expressions of total AKt and phosphorylated AKt were detected by using Western blot test. Results In hypertrophy group, the surface area(1933.80±143.06) and total protein content(367.51±25.9) of myocardial cells were higher than those in control group(787.27±107.66, 218.55±21.28, P0.05), and m RNA expressions of ANP and BNP increased significantly(P0.05). The m RNA expressions of PI3 K, AKt and e NOS and phosphorylated AKt degree decreased in hypertrophy group, and NO release quantity were lower in hypertrophy group(4.60±0.73) than that in control group(8.63±0.30, P0.05). In all M Na HS groups, the hypertrophy effect was inhibited(P0.05) showed a dose-dependent manner after Na HS treating, and the expressions of all signal molecules in PI3K/AKt/e NOS signal pathway were up-regulated(P0.05). ConclusionH2 S had some inhibitory effect on myocardial hypertrophy induced by ET-1, which is related to the activation ofPI3K/AKt/e NOS signal pathway.
Publication Year: 2014
Publication Date: 2014-01-01
Language: en
Type: article
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