摘要
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 effects of angiotensin Ⅱ (Ang Ⅱ ) and angiotensin Ⅱ type Ⅰ receptor antagonist (AT1RA) on contraction of in vitro cultured hepatic stellate cells (HSCs). Methods HSC-T6 hepatic stellate cell line was chosen as the study model of the activated hepatic stellate cells. Cultured HSCs were randomized into the control group, Ang Ⅱ(1 ×10^-9 -1 × 10^-5 )mol/ L groups, AT1RA group and Ang Ⅱ + AT1RA group. The effects of Ang Ⅱ and AT1RA on the hepatic stellate cell contraction were studied by the contraction area of collagen lattice after 48 h. Meanwhile, the dose-effect and time-effect curves were established. Results As compared with the control group, Ang Ⅱ significantly elicited collagen lattice contraction (P〈0. 05). The contractive area of collagen lattice increased along with the concentration of Ang Ⅱ and the dose-effect curve had a positive correlation like a straight line. The contractive area of collagen lattice increased along with the prolongation of Ang Ⅱ action time and the time-effect curve showed the time-dependent manner in 48 h. The levels of the collagen lattice area after 48 h in Ang Ⅱ group and Ang Ⅱ +AT1RA group were 379.337+37.755 mm^2 and 540.803+70.018 mm^2, respectively. ATIRA markedly decreased the contraction of collagen lattice induced by Ang Ⅱ (P〈0. 05). Conclusions Ang Ⅱ can increase the contraction of hepatic stellate cells in a dose- and time-dependent manner while AT1RA inhibits the contraction of hepatic stellate cells induced by Ang Ⅱ.
出处
《中华肝胆外科杂志》
CAS
CSCD
2006年第10期695-698,共4页
Chinese Journal of Hepatobiliary Surgery
基金
本课题受北京市自然科学基金资助(7052024)