一氧化氮合酶/一氧化氮介导人参皂苷Rb1对心肌细胞肥大的抑制效应

目的在血管紧张素Ⅱ(AngⅡ,CoCl2)诱导乳鼠心肌细胞肥大基础上,探讨人参皂苷Rb1(ginsen-oside Rb1,Gs-Rb1)是否可通过一氧化氮合酶/一氧化氮(NOS/NO)系统减轻心肌细胞肥大。方法将乳鼠心肌细胞随机分为对照组、AngⅡ组、Gs-Rb1组、Gs-Rb1+L-NAME(NOS抑制剂)组、Gs-Rb1+AngⅡ+L-NAME组,AngⅡ、L-NAME和Gs-Rb1浓度分别是10μmol/L、1 mmol/L和200μmol/L;分别测定心肌细胞表面积、细胞培养液NO浓度和心肌细胞NOS活性。结果 (1)Gs-Rb1显著抑制AngⅡ所致的心肌细胞肥大(P=0.00),但不能使心肌细胞回复到正常大小;Gs-Rb1减小心肌细胞表面积的效应可被L-NAME显著抑制(P=0.00)。(2)AngⅡ降低心肌细胞NO浓度的效应可被Gs-Rb1显著抑制(P=0.00),但L-NAME可完全抑制Gs-Rb1对心肌细胞的NO分泌效应。(3)Gs-Rb1显著增加心肌细胞在AngⅡ干预时的NOS活性(P=0.00),该效应被L-NAME完全抑制。(4)心肌细胞表面积与NOS(r=0.59,P=0.00)、NO(r=0.62,P=0.00)均呈正相关。结论 Gs-Rb1显著抑制AngⅡ所致的心肌细胞肥大,此效应至少部分通过NOS/NO系统实现。

Ginsenosides-Rb1 inhibits the hypertrophy of cardiomyocytes via Nitric oxide synthase/nitric oxide system

Objective To investigate the inhibition of cardiomyocytes hypertrophy by Ginsenosides-Rb1(Gs-Rb1) via nitric oxide synthase/nitric oxide system(NOS/NO) on the basis of angiotensin Ⅱ(Ang Ⅱ) induced cardiomyocyte hypertrophy in vitro.Methods Neonatal rat cardiomyocytes were randomly divided into control group,Ang Ⅱ group,Gs-Rb1 group,Ang Ⅱ+ L-NAME(nitric oxide synthase inhibitor) group,and Gs-Rb1+Ang Ⅱ+L-NAME group.The concentrations of Ang Ⅱ,Gs-Rb1 and L-NAME were 10 μmol/L,1 mmol/L and 200 μmol/L,respectively.The cell surface area,NO concentration and NOS activity were assayed.Results(1)Gs-Rb1 significantly inhibited cardiomyocyte hypertrophy(P=0.00) mediated by Ang Ⅱ,which was significantly inhibited with L-NAME(P=0.00),though no complete recovery of cell surface area was observed.(2)The Ang Ⅱ-induced down-regulation of NO was significantly alleviated by Gs-Rb1(P=0.00).However,this alleviation was completely eliminated by L-NAME.(3)Gs-Rb1 significantly increased NOS activity in Ang Ⅱ treated cardiomyocytes(P=0.00),however,the effect was completely wiped off by L-NAME.(4)There were significant positive correlations between cell surface area and NOS activity(r=0.59,P=0.00),and NO(r=0.62,P=0.00).Conclusion Gs-Rb1 inhibits Ang Ⅱ-induced cardiomyocyte hypertrophy,which is partially mediated by NOS/NO system.