优化后的新圣麦粉通过调节大鼠肉瘤/快速加速纤维肉瘤/介原激活蛋白激酶激酶/胞外调控蛋白激酶信号通路,抑制心衰患者的心肌纤维化。

Zhang Zeyu, Jia Zhuangzhuang, Song Yuwei, Zhang Xuan, Wang Ci, Wang Shuai, Zhang Peipei, Ren Qiuan, Wang Xianliang, Mao Jingyuan
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引用次数: 0

摘要

目的方法:将70只Sprague-Dawley大鼠随机分为假组(n=10)和手术组(n=60),通过结扎大鼠左前降支建立心衰大鼠的心肌纤维化:将 70 只 Sprague-Dawley 大鼠随机分为假手术组(n = 10)和手术组(n = 60),然后通过结扎冠状动脉左前降支建立高频大鼠。我们将手术组大鼠随机分为模型组、ONSMP(包括低剂量(L)、中剂量(M)和高剂量(H))组和依那普利组。在为期 4 周的药物干预后,超声心动图检查心脏功能,并计算全心/左心与大鼠体重的比率。最后,我们通过病理切片观察心肌纤维化的程度,用酶联免疫吸附法测定心肌胶原蛋白(COL)Ⅰ和COLⅢ的含量,检测COLⅠ、COLⅢ、α-平滑肌肌动蛋白(α-SMA)的mRNA水平、并通过Western blot检测p-RAS、p-RAF、p-MEK1/2、p-ERK1/2、p-ETS-like-1转录因子(p-ELK1)、p-c-Fos、α-SMA、COLⅠ和COLⅢ的蛋白表达。结果ONSMP能有效改善HF大鼠的心功能,降低心器官系数、COL体积分数和COLⅠ/Ⅲ含量,下调COLⅠ/Ⅲ、α-SMA和c-Fos的mRNA,以及p-RAS、p-RAF、p-MEK1/ 2、p-ERK1/2、p-ELK1、c-Fos、COLⅠ/Ⅲ和α-SMA的蛋白:结论:ONSMP能有效减轻高频大鼠的心肌纤维化,其机制可能与抑制RAS/RAF/MEK/ERK信号通路有关。
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Optimized new Shengmai powder inhibits myocardial fibrosis in heart failure by regulating the rat sarcoma/rapidly accelerated fibrosarcoma/mitogen-activated protein kinase kinase/extracellular regulated protein kinases signaling pathway.

Objective: Exploring the effect of Optimized New Shengmai powder (, ONSMP) on myocardial fibrosis in heart failure (HF) based on rat sarcoma (RAS)/rapidly accelerated fibrosarcoma (RAF)/mitogen-activated protein kinase kinase (MEK)/extracellular regulated protein kinases (ERK) signaling pathway.

Methods: Randomized 70 Sprague-Dawley rats into sham (n = 10) and operation (n = 60) groups, then established the HF rat by ligating the left anterior descending branch of the coronary artery. We randomly divided the operation group rats into the model, ONSMP [including low (L), medium (M), and high (H) dose], and enalapril groups. After the 4-week drug intervention, echocardiography examines the cardiac function and calculates the ratios of the whole/left heart to the rat's body weight. Finally, we observed the degree of myocardial fibrosis by pathological sections, determined myocardium collagen (COL) I and COL Ⅲ content by enzyme-linked immunosorbent assay, detected the mRNA levels of COL I, COL Ⅲ, α-smooth muscle actin (α-SMA), and c-Fos proto-oncogene (c-Fos) by universal real-time, and detected the protein expression of p-RAS, p-RAF, p-MEK1/2, p-ERK1/2, p-ETS-like-1 transcription factor (p-ELK1), p-c-Fos, α-SMA, COL I, and COL Ⅲ by Western blot.

Results: ONSMP can effectively improve HF rat's cardiac function, decrease cardiac organ coefficient, COL volume fraction, and COL I/Ⅲ content, down-regulate the mRNA of COL I/Ⅲ, α-SMA and c-Fos, and the protein of p-RAS, p-RAF, p-MEK1/ 2, p-ERK1/2, p-ELK1, c-Fos, COL Ⅰ/Ⅲ, and α-SMA.

Conclusions: ONSMP can effectively reduce myocardial fibrosis in HF rats, and the mechanism may be related to the inhibition of the RAS/RAF/MEK/ERK signaling pathway.

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