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目的观察血管紧张素Ⅱ及其受体拮抗剂对体外培养的肝星状细胞收缩的影响。方法采用HSC-T6肝星状细胞系作为活化的肝星状细胞的研究模型。将培养的肝星状细胞随机分为对照组、血管紧张素Ⅱ(1×10-9～1×10-5)mol／L组、受体拮抗剂组和血管紧张素Ⅱ+受体拮抗剂组,继续培养48 h后,比较胶原晶格收缩面积的变化,并绘制收缩的量效关系曲线和时效关系曲线。结果血管紧张素Ⅱ各浓度组,胶原晶格的收缩面积比较对照组均明显增加(P<0．05)。随着血管紧张素Ⅱ浓度的升高,胶原晶格的收缩面积逐渐增大,量效曲线呈近似直线的正相关关系;而且随着血管紧张素Ⅱ作用时间的延长,胶原晶格的收缩面积逐渐增大,在48 h之内呈时间依赖性。血管紧张素Ⅱ作用48 h后,胶原晶格面积为(379．337±37．755)mm2,同时加入受体拮抗剂,面积为(540．803±70．018)mm2,胶原晶格的收缩程度比较血管紧张素Ⅱ组明显减轻(P<0．05)。结论血管紧张素Ⅱ能够剂量依赖性和时间依赖性地促进肝星状细胞的收缩,而血管紧张素Ⅱ1型受体拮抗剂能够抑制血管紧张素Ⅱ引起的肝星状细胞的收缩。
Objective To investigate the effect of angiotensin Ⅱ and its receptor antagonist on the contraction of hepatic stellate cells cultured in vitro. Methods HSC-T6 hepatic stellate cell line was used as a model of activated hepatic stellate cells. The cultured hepatic stellate cells were randomly divided into control group, angiotensin Ⅱ (1 × 10-9 ~ 1 × 10-5) mol / L group, receptor antagonist group and angiotensin Ⅱ receptor antagonist Group, continue to cultivate after 48 h, compare the contractile area of collagen lattice changes, and draw the contraction of the dose-effect relationship curve and the relationship between the aging curve. Results Compared with the control group, the contractile area of collagen lattice in each concentration of angiotensin Ⅱ group was significantly increased (P <0.05). As the concentration of angiotensin Ⅱ increased, the contractile area of collagen lattice gradually increased, and the dose-response curve showed a nearly linear positive correlation. With the prolongation of angiotensin Ⅱ, the contractile area of collagen lattice Gradually increased, within a time-dependent manner within 48 h. Angiotensin Ⅱ treated for 48 h, the area of collagen was (379.337 ± 37.755) mm2, and the area of receptor antagonist was (540.803 ± 70.018) mm2. Collagen lattice contraction The degree of angiotensin Ⅱ group was significantly reduced (P <0.05). Conclusion Angiotensin Ⅱ can promote hepatic stellate cell contraction in a dose - dependent and time - dependent manner. Angiotensin Ⅱ type 1 receptor antagonist can inhibit the contraction of hepatic stellate cells induced by angiotensin Ⅱ.