大理大学学报 ›› 2021, Vol. 6 ›› Issue (2): 55-58.DOI: 10. 3969 / j. issn. 2096-2266. 2021. 02. 011

• 基础医学 • 上一篇    下一篇

Cx26在D-半乳糖胺诱导的急性肝损伤中的表达

王斌1,赖硕林2,宋豫皎2,何欣然2,王烨婷2,赵钐妤3*   

  1. (1.大理大学第一附属医院,云南大理671000;2.大理大学临床医学院,云南大理671000;
    3. 大理大学基础医学院,云南大理671000)
  • 收稿日期:2020-06-16 修回日期:2020-09-16 出版日期:2021-02-15 发布日期:2021-03-17
  • 通讯作者: 赵钐妤,讲师,E-mail:zhaoshanyu2011@163.com。
  • 作者简介:王斌,主管药师,主要从事临床药学研究。
  • 基金资助:
    云南省应用基础研究计划项目(2017FD138)

Expression of Cx26 in Acute Liver Injury Induced by D-galactosamine

Wang Bin1, Lai Shuolin2, Song Yujiao2, He Xinran2, Wang Yeting2, Zhao Shanyu3*   

  1. (1. The First Affiliated Hospital of Dali University, Dali, Yunnan 671000, China; 2. Clinical College, Dali University,
    Dali, Yunnan 671000, China; 3. Pre-clinical College, Dali University, Dali, Yunnan 671000, China)
  • Received:2020-06-16 Revised:2020-09-16 Online:2021-02-15 Published:2021-03-17

摘要: 目的:研究连接蛋白Cx26在D-半乳糖胺诱导的大鼠急性肝损伤中的表达及意义。方法:建立D-半乳糖胺诱导大鼠急
性肝损伤模型,用联苯双酯干预作为阳性对照组,检测肝体比指数、血清中天门冬氨酸氨基转移酶(AST)和丙氨酸氨基转移酶
(ALT)的含量;采用显微镜观察大鼠肝脏的病理改变;采用蛋白印迹法(WB)对Cx26蛋白进行定量分析;用实时荧光定量聚合
酶链反应(Real-time qPCR)检测Cx26的mRNA表达情况。结果:D-半乳糖胺引起大鼠肝脏急性损伤,可见细胞坏死,引发炎
症反应;AST、ALT含量明显升高(P < 0.05);Cx26的蛋白含量显著增加(P < 0.05),而其mRNA的含量明显减少(P < 0.01)。给
予联苯双酯干预后,未改变D-半乳糖胺所致肝损伤时Cx26蛋白及mRNA的异常表达。结论:D-半乳糖胺可致大鼠肝脏中
Cx26表达异常,这可能是其致病机理之一,可为肝损伤的治疗提供一个潜在的靶点。

关键词: 连接蛋白, Cx26, 急性肝损伤, D-半乳糖胺

Abstract: Objective: To study the effect of Connexin(Cx)26 on acute liver injury induced by D-galactosamine in rats. Methods:
To establish the model of acute liver injury induced by D-galactosamine, bifendatatum was used as positive drug. The liver-body
ratio, serum aspartate aminotransferase(AST)and alanine aminotransferase(ALT)levels were measured. Pathological changes were
observed by microscope. Cx26 protein was quantitatively analyzed by Western Blot(WB). The mRNA expression of Cx26 was
detected by real-time quantitative polymerase chain reaction (Real-time qPCR). Results: D-galactosamine caused acute liver
injury, cell necrosis was observed and inflammatory reaction was induced. The content of AST and ALT was significantly increased
(P < 0.05). The protein content of Cx26 in the liver increased significantly (P < 0.05), while the mRNA content decreased
significantly(P < 0.01). Intervention with bifendatatum did not reverse the damage caused by D-galactosamine and the abnormal
expression of Cx26. Conclusion: D-galactosamine can cause abnormal increase of Cx26 protein expression in rat liver, which may be
one of the pathogenic mechanisms, and also provide a potential target for the treatment of liver injury.

Key words: connexin, Cx26, acute liver injury, D-galactosamine

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