【摘要】 目的探讨Rho激酶通路的激活对血管紧张素I(IAng II)诱导的人气道平滑肌细胞(human airway smooth musclecells,HASMCs)收缩的作用及其机制。方法原代培养人气道平滑肌细胞,分为对照组、AngII组、AngII+伊贝沙坦[AngII1型受体(AT1R)阻断剂,IRB]组、AngII+Y-27632(Rho激酶抑制剂)组分别用胶原收缩法、免疫荧光等从细胞形态检测AngII对细胞收缩的影响及Western Blot在蛋白水平上检测Rho激酶通路蛋白的变化。结果 Y-27632、伊贝沙坦均可显著抑制AngI(I10-7 mol/L)诱导的人气道平滑肌细胞收缩,两组的抑制作用无显著差异(P>0.05);Y-27632对AngII诱导的Rho激酶底物磷酸化moesin的表达的抑制作用显著高于伊贝沙坦(P<0.05)。结论 AngII诱导的HASMCs收缩可能与Rho激酶通路的激活有关。更多还原

【Abstract】 Objective To investigate of the regulatory effect of Rho-kinase pathway activation on angiotensin II(Ang II)-induced contraction of human airway smooth muscle cells(HASMCs) in vitro.Methods Cultured primary HASMCs were divided into control group,AngII group,AngII + irbesartan group and AngII + Y-27632 group with corresponding treatment.AngII-induced contraction of HASMCs was evaluated using collagen gel lattices and observed morphologically using immunofluorescence assay.Western Blotting was significantly performed to examine the protein expression of Rho-kinase signal pathway.Results AngII-induced HASMC contraction was inhibited by treatments with irbesartan and Y-27632 as shown by gel contraction assay(P<0.001).Y-27632 treatment produced a stronger inhibitory effect than irbesartan on the expression of phosphorylated moesin,a substrate of Rho kinase(P<0.05).Conclusion AngII induces the contraction of HASMCs partially as a result of activation of Rho-kinase pathway.更多还原