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作 者:张军[1] 张忠涛[1] 王宇[1] 王萍[2] 唐淑珍[2] 周延忠[1] 李建设[1]
机构地区:[1]首都医科大学附属北京友谊医院普外科,北京市100050 [2]首都医科大学附属北京友谊医院病生理实验室,北京市100050
出 处:《中华肝胆外科杂志》2005年第12期848-850,共3页Chinese Journal of Hepatobiliary Surgery
基 金:北京市重点学科项目资助(1998卫科扶字11号)
摘 要:目的研究内皮素及其受体拮抗剂对肝星状细胞(hepatic stellate cell,HSC)的收缩作用及其作用的受体机制。方法采用胶原晶格法(collagen lattice)观察ET-1及其受体拮抗剂BQ-123、BQ-788和选择性ETB受体协同剂IRL-1620对肝星状细胞收缩的影响。结果与空白对照组相比,ET-1组和ET-1+BQ-788组收缩面积百分比显著降低(0·504±0·082vs0·848±0·038,P<0·05;0·498±0·102vs0·848±0·038,P<0·05),而ET-1+BQ-123组则无明显差异(0·865±0·025vs0·848±0·038,P>0·05);与空白对照组相比,ET-110nmol/L+IRL-16201μmol/L组收缩面积百分比显著降低(0·429±0·117vs0·758±0·036,P<0·05),而ET-1100pmol/L+IRL-16201μmol/L组与空白对照组无差异(0·724±0·061vs0·758±0·036,P>0·05)。结论内皮素-1引起肝星状细胞的收缩是由内皮素受体A介导的,选择性内皮素受体A拮抗剂BQ-123可以抑制内皮素-1介导的肝星状细胞的收缩,而内皮素B受体拮抗剂则无此作用;选择性内皮素B受体协同剂IRL-1620能抑制较低浓度的ET-1引起的肝星状细胞的收缩。Objective To study the effects of endothelin and its antagonists on contractility of HSC-T6 cells. Methods Collagen lattice was used to investigate the effects of endothelin-1 (ET-1), selective ETA receptor antagonist BQ-123, selective ETB receptor antagonist BQ-788 and selective ETB receptor synergist IRL-1620 on contractility of hepatic stellate cells. Results The percentage of contracting area in ET-1 group and ET-1 + BQ-788 group was obviously lower than that in control group and ET-1+BQ-123 group (P〈0. 05). Using ET-1 together with BQ-123 could obviously inhib- it the contractility of HSC. BQ-788 had no significant effect of inhibiting the contractility. The con- tracting area percentage in ET-1 10nM+IRL-1620 1μM group was markedly lower than that in the control group (P〈0.05). However, there was no significant difference in percentage between ET-1 100pM+IRL-1620 1μM group and the control group (P〈0.05). IR-1620 could inhibit the contractility induced by 100pM ET-1. However, this action was not obvious in ET-1 10nM group. Conclusions BQ-123 can significantly inhibit HSC contractility induce by endothelin. But BQ-788 has no such effect. ETA receptor can induce the contractility of HSC. IRL-1620 can inhibit HSC contractility induced by low level of ET-1.
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