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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 mechanism of endothelin and its receptor antagonist on hepatic stellate cell (HSC) contraction and its receptor mechanism. Methods collagen lattices were used to observe the effects of ET-1 and its receptor antagonists BQ-123, BQ-788 and selective ETB receptor synergist IRL-1620 on hepatic stellate cell contraction. Results Compared with the blank control group, the percentages of contractile area in ET-1 group and ET-1 + BQ-788 group were significantly decreased (0 · 504 ± 0 · 082 vs 0 · 848 ± 0 · 038, P <0.05 · 0.498 ± 0 · 102vs0 · 848 ± 0 · 038, P <0 · 05), but there was no significant difference between the ET-1 + BQ-123 group (0 · 865 ± 0 · 025vs0 · 848 ± 0 · 038, P> 0 · Compared with the blank control group, the percentage of contracted area in ET-110nmol / L + IRL-16201μmol / L group was significantly lower than that in the blank control group (0.42.9 ± 0.117 vs0.775 ± 0.036, P <0.05) No difference was found between ET-1100pmol / L + IRL-16201μmol / L group and blank control group (0 · 724 ± 0 · 061vs0 · 758 ± 0 · 036, P> 0.05). Conclusion Endothelin-1-induced hepatic stellate cell contraction is mediated by endothelin receptor-A, and selective endothelin receptor A antagonist BQ-123 inhibits endothelin-1-mediated hepatic stellate cell contraction , Whereas endothelin B receptor antagonist did not; and selective endothelin B receptor synergist IRL-1620 inhibited hepatic stellate cell contraction induced by lower concentrations of ET-1.