基础医学与临床 ›› 2018, Vol. 38 ›› Issue (9): 1251-1257.

• 研究论文 • 上一篇    下一篇

内皮间质转化参与阿霉素诱导的大鼠心肌纤维化

邓飞艳1,2,谢路远1,2,詹世斌1,刘志燕1,薛蕾1,高妮娜1,盛小伍1   

  1. 1. 湖南省肿瘤医院
    2. 南华大学
  • 收稿日期:2018-01-15 修回日期:2018-05-30 出版日期:2018-09-05 发布日期:2018-09-10
  • 通讯作者: 盛小伍 E-mail:shengxiaowu789@163.com
  • 基金资助:
    血液系统常用化疗药物对脂肪干细胞的影响研究

Endothelial to mesenchymal transition participates in doxorubicin induced rat myocardial fibrosis

  • Received:2018-01-15 Revised:2018-05-30 Online:2018-09-05 Published:2018-09-10
  • Contact: Xiao-Wu Sheng E-mail:shengxiaowu789@163.com

摘要: 目的 研究阿霉素对心肌纤维化形成的机制。方法 构建大鼠阿霉素心肌纤维化模型,HE染色和Masson染色检测心肌病理变化,RT-qPCR和免疫组化检测纤维化相关基因Col1α、Col3α和TGF-β1的表达。免疫荧光技术检测心肌组织内皮细胞标志物vWF和间质细胞标志物α-SMA的表达。结果 给大鼠腹腔注射阿霉素(2mg/kg,每周1次。)出现心室腔扩大、心壁变薄、心肌纤维间隙增宽、心肌溶解、心肌纤维化、心肌血管内皮损伤和通透性增加。随着阿霉素作用时间延长实验组相比于对照组心肌纤维化程度明显(P<0.05),纤维化相关因子Col1α、Col3α和TGF-β1的表达增多(P<0.05),阿霉素心肌纤维化大鼠心脏血管内皮细胞出现内皮间质转化。结论 阿霉素可诱导大鼠不可逆的心肌纤维化,内皮间质转化参与阿霉素心肌纤维化的形成。

关键词: 内皮间质转化,心肌纤维化,肿瘤坏死因子,转化生长因子β,平滑肌肌动蛋白

Abstract: Objective To study the of mechanism of adriamycin induced myocardial fibrosis .Methods Construct rat model of doxorubicin induced myocardial fibrosis. Detect the myocardial pathological changes with HE and Masson staining, and detect the expression level of fibrosis related gene Col1α, Col3α, TGF-β1 with RT-qPCR and immunohistochemistry. The immunofluorescence technique was used to detect the expression of the marker of vascular endothelial cell (vWF) and mesenchymal cell (α-SMA). Results Enlargement of ventricular cavity, thinning of heart wall, widening of myocardial fiber space, myocardial dissolving and fibrosis, myocardial vascular endothelial injury and permeability increase happened in rats with intraperitoneal injection of adriamycin. With the prolonged action of adriamycin, the expression of myocardial fibrosis factors and fibrosis related factors Col1α、Col3α、TGF-β1 increased, endothelial cell transformation happened in cardiac vascular endothelial cells. Conclusion Adriamycin can induce irreversible myocardial fibrosis in rats, and endothelium transformation is involved in the formation of doxorubicin induced myocardial fibrosis.

Key words: Endothelial to Mesenchymal Transition(EndoMT), Cardiac fibrosis, TNF-α, TGFβ,α-SMA

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