中国畜牧兽医

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马兜铃酸肾病中相关因子的表达变化

田娅慧1,常迪1,杨耀晖1,吴国英2,赵海焦1,吴金栋1,吴国娟1,张中文1   

  1. 1.北京农学院动物科学技术学院,北京 102206;2.吉林省长春市双阳区妇幼保健所,吉林长春 130600
  • 收稿日期:2014-04-29 出版日期:2014-08-20 发布日期:2014-08-22
  • 通讯作者: 国娟(1956—),女,教授,研究方向:中药药理与毒理。E-mail:wgj9288@sina.com;Tel:010-80796702 张中文,男,教授。E-mail:zwzhang9288asina.com;Tel:010-80799146
  • 作者简介:田娅慧(1989—),女,河北人,硕士,研究方向:兽医药理学。 常迪(1989—),女,北京人,硕士生,研究方向:兽医药理与毒理。 田娅慧与常迪对本文具有同等贡献,并列为第一作者。
  • 基金资助:

    国家基金(31172362);北京农学院2013年科研质量提高经费(高质量论文招标项目GZL2013004);兽医学(中医药)北京市重点实验室;农业应用新技术北京市重点实验室;北京市属高等学校创新团队建设与教师职业发展计划项目——创新团队提升计划“肉牛种质创新与利用”(PXM2013_014207_000067)。

Expression Changes of Relative Factors in Mice with Aristolochic Acid Nephropathy

TIAN Ya-hui1, CHANG Di1, YANG Yao-hui1, WU Guo-ying2, ZHAO Hai-jiao1, WU Jin-dong1, WU Guo-juan1, ZHANG Zhong-wen1   

  1. 1. Department of Animal Science and Technology, Beijing University of Agriculture, Beijing 102206, China; 2. Maternity and Child Care Center, Shuangyang District, Changchun City, Jilin Province, Changchun 130600, China
  • Received:2014-04-29 Online:2014-08-20 Published:2014-08-22

摘要: 本研究旨在探讨马兜铃酸肾病(AAN)中标志性因子的表达变化。30只小鼠灌胃8 mg/(kg·d) 马兜铃酸Ⅰ(AAⅠ),于不同时间处死,用常规病理切片染色法观察肾脏不同时间段的病理变化程度,以实时荧光定量PCR和Western blotting检查各组小鼠肾组织细胞标志性蛋白α-平滑肌肌动蛋白(α-SMA)、角蛋白18(CK-18)、波形蛋白(vimentin)的表达变化。结果显示随着AAⅠ用药时间的延长,肾脏损伤逐渐加重,并证实AAⅠ可诱导小鼠肾脏发生上皮—间质转分化(EMT),促进α-SMA、vimentin的mRNA及蛋白表达增加,抑制CK-18的表达,为AAN更深一步的机制研究提供有力的理论基础。

关键词: 马兜铃酸肾病; α -SMA; vimentin; CK-18

Abstract: The study was aimed to observe the expression changes of relative factors in mice with aristolochic acid nephropathy (AAN). 30 mice were given aristolochic acid Ⅰ (AAⅠ) at 8 mg/(kg·d), and mice were killed at a different time. Then observe the renal pathological changes by hematoxylin-eosin (H&E), Real-time PCR and Western blotting technology were used to detect the expression changes of α-SMA, vimentin and CK-18. The results showed that with the extension of treatment time, we could found the kidney structure was damaged more seriously, and confirmed that AAⅠcould induce epithelial-mesenchymal transition (EMT) in renal, promoted the expression of α-SMA and vimentin, inhibited the expression of CK-18. The study laid a foundation for a deeper mechanism study of AAN.

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