Sun Rongrong, Wang Jiangbo, Zheng Yi, Li Xianchi, Xie Tiantian, Li Rui, Liu Min, Cao Yong, Lu Lei, Zhang Qing, Zhang Peiying
Clinical Medicine, Nanjing University of Traditional Chinese Medicine, The Affiliated Xuzhou Central Hospital of Nanjing University of Traditional Chinese Medicine, Nanjing, Jiangsu 210023, P.R. China.
Department of Neurology, Xuzhou Central Hospital, Xuzhou, Jiangsu 221009, P.R. China.
Exp Ther Med. 2017 May;13(5):1900-1906. doi: 10.3892/etm.2017.4223. Epub 2017 Mar 10.
We investigated the effect of baoxin decoction (BXD) on myocardial fibrosis and clarified the possible mechanism of action. Dilated myocardiopathy was induced by doxorubicin injected intraperitoneally for 6 weeks. Rats that demonstrated dilated myocardiopathy were randomly divided into five groups plus a control group. Three groups were treated with BXD (7.5/kg, 15 g/kg and 30 g/kg) daily for 4 weeks. One group was treated with 8.75 g/kg of captopril (positive control), and with physiologic saline (negative control). Cardiac function was evaluated using echocardiography. Hematoxylin and eosin, and Massons trichrome staining were performed, PICP and PIIINP were assessed by ELISA, the expression of galectin-3 and collagen types I and III was evaluated with reverse transcription-quantitative PCR, and interrelated proteins were detected by western blot analysis. BXD downregulated galectin-3, collagen I and III and was correlated with a high expression of fibrosis markers. It also significantly decreased myocardial collagen volume fraction (CVF), together with markedly preventing the upregulation of collagen I and III. In addition, BXD downregulated the expression of TGF-β1 and Smad3 in the myocardial fibrosis rats. Therefore, BXD treatment significantly improved cardiac function and alleviated myocardial fibrosis in a rat model of doxorubicin-induced dilated cardiomyopathy (DCM), which is the mechanism that may be associated with inhibiting the TGF-β1 signaling pathway.
我们研究了保心汤（BXD）对心肌纤维化的影响，并阐明了其可能的作用机制。通过腹腔注射阿霉素6周诱导扩张型心肌病。将表现出扩张型心肌病的大鼠随机分为五组加一个对照组。三组大鼠每天接受BXD治疗（7.5/kg、15 g/kg和30 g/kg），持续4周。一组大鼠接受8.75 g/kg卡托普利治疗（阳性对照），另一组接受生理盐水治疗（阴性对照）。使用超声心动图评估心脏功能。进行苏木精-伊红染色和Masson三色染色，通过酶联免疫吸附测定法评估血清前胶原Ⅲ肽（PICP）和Ⅲ型前胶原氨基端肽（PIIINP），用逆转录定量聚合酶链反应评估半乳糖凝集素-3及Ⅰ型和Ⅲ型胶原蛋白的表达，并用蛋白质印迹分析检测相关蛋白。BXD下调了半乳糖凝集素-3、Ⅰ型和Ⅲ型胶原蛋白的表达，且与纤维化标志物的高表达相关。它还显著降低了心肌胶原容积分数（CVF），同时明显抑制了Ⅰ型和Ⅲ型胶原蛋白的上调表达。此外，BXD下调了心肌纤维化大鼠中转化生长因子-β1（TGF-β1）和Smad3蛋白的表达。因此，在阿霉素诱导性扩张型心肌病（DCM）大鼠模型中，BXD治疗显著改善了心脏功能并减轻了心肌纤维化，其机制可能与抑制TGF-β1信号通路有关。
