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中国临床药理学与治疗学 ›› 2008, Vol. 13 ›› Issue (5): 499-503.

• 基础研究 • 上一篇    下一篇

雷公藤甲素抑制血管紧张素Ⅱ诱导的心肌成纤维细胞增殖及胶原合成的研究

徐朝军1, 宋岚2, 尹晓清1, 郭正宇1, 杨进1   

  1. 1湖南中医药大学第一附属医院胸心外科, 长沙410007, 湖南;
    2南华大学生物化学与分子生物学教研室, 衡阳421001, 湖南
  • 收稿日期:2008-02-29 修回日期:2008-04-28 发布日期:2020-11-09
  • 作者简介:徐朝军, 男, 博士, 讲师, 主治医师, 主要从事心血管疾病研究。Tel:0731-5369067 E-mail:xuzhaojun1492 @yahoo.com. cn
  • 基金资助:
    湖南省科技厅基金项目(2007FJ4290)

Influence of triptolide on the proliferation and pro α1(Ⅰ) collagen synthesis in cultured neonatal rat myocardial fibroblast stimulated by angiotensin Ⅱ

XU Zhao-jun1, SONG Lan1, YIN Xiao-qing1, GUO Zheng-yu1, YANG Jing1   

  1. 1Department of Cardiothoracic Surgery, First Affiliated Hospital, HunanUniversity of Traditional Chinese Medicine,Changsha 410007, Hunan, China;
    2Department of Molecular Biology and Biochemistry, Nanhua University,Hengyang 421001, Hunan, China
  • Received:2008-02-29 Revised:2008-04-28 Published:2020-11-09

摘要: 目的:探讨雷公藤甲素对血管紧张素Ⅱ(Ang Ⅱ) 诱导的新生大鼠心肌成纤维细胞(cardiacfibroblasts,CFb) 增殖及α1(Ⅰ) 型前胶原合成的影响。方法:建立Ang Ⅱ诱导新生大鼠心肌纤维化细胞模型。采用四氮唑蓝(MTT) 比色法测定细胞增殖;分别采用逆转录聚合酶链反应(RT-PCR)和Western blot 印迹法检测大鼠心肌成纤维细胞α1(Ⅰ) 型前胶原mRNA 及蛋白表达。结果:雷公藤甲素以剂量依赖性方式抑制心肌成纤维细胞增殖和α1(Ⅰ) 型前胶原合成。结论:雷公藤甲素可以通过抑制Ang Ⅱ诱导的心肌成纤维细胞增殖和α1(Ⅰ) 型前胶原合成从而抑制心肌纤维化。

关键词: 雷公藤甲素, 心肌成纤维细胞, 血管紧张素Ⅱ, α1(Ⅰ) 型前胶原

Abstract: AIM:To study the influence of triptolide on the angiotension Ⅱ(Ang Ⅱ)-induced neonatalrat myocardial fibroblasts (CFb) proliferation and pro α1(Ⅰ) collagen synthesis, and to explore the mecha-nism triptolide on myocardial fibrosis. METHODS: Neonatal rat myocardial fibroblasts were treated with 1×10-7 mmol/L angiotensin Ⅱ (Ang Ⅱ, 1 ×10-7mmol/L) to make fibrosis model. The inhibition of triptolide on CFb proliferation was evaluated by MTT assay, the synthesis of pro α1(Ⅰ) collagen was observed by RT-PCR and Western blotting. RESULTS: In a concentration range, triptolide (0. 5, 1. 0, 2. 0 and 4. 0 μg/mL) significantly inhibited the Ang Ⅱ-induced CFb proliferation and pro α1(Ⅰ) collagen synthsis in a dose-dependent way. CONCLUSION: Triptolide might attenuate myocardial fibrosis induced by angiotensin Ⅱ through inhibiting CFb proliferation and pro α1(Ⅰ) collagen synthsis.

Key words: triptolide, myocardial fibroblast, angiotensin Ⅱ, pro α1(Ⅰ) collagen

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