Role of PI3K/AKt/eNOS signal pathway in course of H2S inhibiting myocardial hypertrophy induced by ;ET-1
WANG Ya-jing
ZHANG Xue-zhi
DIAO Li
WANG Qi-xin
Abstract：Objective To observe the role of PI3K/AKt/eNOS signal pathway in course of H2S 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, ② hypertrophy group, with 10-8 mol/l ET-1, ③10-15 M NaHS group, with 10-15 mol/l NaHS+10-8 mol/l ET-1,④10-14 M NaHS group, with 10-14 mol/l NaHS+10-8 mol/l ET-1, ⑤10-13 M NaHS group, with 10-13 mol/l NaHS+10-8 mol/l ET-1, and ⑥10-12 M NaHS group, with 10-12 mol/l NaHS+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 mRNA 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 (eNOS) 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, P<0.05), and mRNA expressions of ANP and BNP increased significantly (P<0.05). The mRNA expressions of PI3K, AKt and eNOS 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, P<0.05). In all M NaHS groups, the hypertrophy effect was inhibited (P<0.05) showed a dose-dependent manner after NaHS treating, and the expressions of all signal molecules in PI3K/AKt/eNOS signal pathway were up-regulated (P<0.05). Conclusion H2S had some inhibitory effect on myocardial hypertrophy induced by ET-1, which is related to the activation of PI3K/AKt/eNOS signal pathway.
Keywords：Hydrogen sulfideProtein kinase BEndothelial nitric oxide synthaseEndothelin-1Myocardial hypertrophy
Publication Date：2014-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：5( 551-554,557 )