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目的:探讨肝组织中的α1-烟碱样乙酰胆碱受体在胆汁性肝纤维化引起的门静脉高压症(PHT)发病机制中的作用。方法:取体重240-260g的清洁级雄性SD大鼠30只,根据体重随机分为假手术组、模型组。模型组采用胆总管结扎术(CBDL)对大鼠进行造模,分别于2周、4周测门静脉压力,并用免疫组化和免疫印迹法对α1-烟碱样乙酰胆碱受体(nAchRα1)进行定位及定量的检测。结果:假手术组的门静脉压力是7.97±0.55mmHg,造模后2周和4周门静脉压力升高,分别为14.15±0.92mmHg;17.75±0.86mmHg。免疫组化显示nAchRα1主要表达在肝窦和汇管区。免疫印迹显示模型组nAchRα1的表达较假手术组明显增多。结论:nAchRα1可能通过活化肝星状细胞,进而形成肝窦毛细血管化,来参与门静脉高压症的发病机制。
Objective: To investigate the role of α1-nicotinic acetylcholine receptor in liver tissue in the pathogenesis of portal hypertension (PHT) induced by biliary liver fibrosis. Methods: Thirty male SD rats weighing 240-260g were randomly divided into sham operation group and model group according to body weight. The rats in model group were treated by common bile duct ligation (CBDL). The pressure of portal vein was measured at 2 weeks and 4 weeks respectively. The nAChRα1 (α1-nicotinic acetylcholine receptor) was localized by immunohistochemistry and immunoblotting And quantitative testing. Results: The portal vein pressure in the sham operation group was 7.97 ± 0.55mmHg, and the portal vein pressure increased 14.15 ± 0.92mmHg and 17.75 ± 0.86mmHg at 2 and 4 weeks after modeling. Immunohistochemistry showed that nAchRα1 was mainly expressed in sinusoids and portal area. Immunoblotting showed that the expression of nAchRα1 in the model group was significantly increased compared with the sham operation group. Conclusion: nAchRα1 may participate in the pathogenesis of portal hypertension by activating hepatic stellate cells and then forming hepatic sinusoidal capillaries.