基础医学与临床 ›› 2018, Vol. 38 ›› Issue (5): 626-631.

• 研究论文 • 上一篇    下一篇

β1-肾上腺素受体自身抗体通过促进肝细胞凋亡参与小鼠肝损伤

于海存1,杜芸辉1,张诗晗1,闫莉2,李玉明3   

  1. 1. 首都医科大学
    2. 中国医学科学院基础医学研究所
    3. 首都医科大学燕京医学院
  • 收稿日期:2017-10-16 修回日期:2018-03-20 出版日期:2018-05-05 发布日期:2018-04-28
  • 通讯作者: 李玉明 E-mail:ymlea@sina.com
  • 基金资助:
    国家自然科学基金;国家自然科学基金;北京市自然科学基金

Hepatocytes apoptosis induced by β1-adrenoceptor autoantibody iis nvolved in hepatic dysfunction

  • Received:2017-10-16 Revised:2018-03-20 Online:2018-05-05 Published:2018-04-28

摘要: 目的 探讨β1-肾上腺素受体自身抗体(β1-AA)对小鼠肝功能的影响。方法 用杂交瘤细胞株融合的方法产生具有生物活性的β1-AA;构建β1-AA长期被动免疫小鼠模型;血清生化仪检测肝脏血清学指标变化;超声检测小鼠肝脏结构和功能的改变;Tunel染色、Annexin V/PI染色和caspase 3活性检测肝细胞凋亡水平。结果 具有生物活性的β1-AA和被动免疫模型小鼠建立成功;在被动免疫过程中,免疫组小鼠肝脏ALT(62.00 ± 0.01 v.s. 37.00 ± 0.02),AST(290.00 ± 0.05 v.s. 205.00 ± 0.02)水平明显升高,ALB显著下降(35.00 ± 0.03 v.s. 43.00 ± 0.05);门静脉、肝静脉流速降低;β1-AA长期存在诱导肝细胞凋亡水平增加(8.00% ± 0.02% v.s. 2.30% ± 0.03%,P<0.05),β1-肾上腺素受体特异性抑制剂metoprolol可以部分逆转此效应。结论 β1-AA可以通过β1-肾上腺素受体致肝细胞凋亡,参与肝损伤的发生发展。

关键词: β1-肾上腺素受体 自身抗体 肝细胞 凋亡

Abstract: Objective To investigate the effect of β1-Adrenoceptor autoantibody on liver function. Methods The biologically active of β1-AA was prepared and passive immunization model was established with β1-AA. The biochemical parameters of the liver were measured by the automatic serum biochemical analyzer. The liver size, hepatic vein, portal vein velocity were detected by liver ultrasound; hepatocytes apoptosis were tested by tunel staining, Annexin V / PI staining and caspase 3 activity detection. Results The biologically active of β1-AA and passive immunization model were established successfully. The ALT and AST of the liver significantly increased and the ALB decreased in the passive immunization process. The apoptosis of the hepatocytes increased, and metoprolol could partially reversed this effect. Conclusion β1-AA can induce hepatocytes apoptosis by β1-adrenergic receptor and participate in the development of liver injury.

Key words: β1-adrenergic receptor autoantibody hepatic cells apoptosis

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