Liu Qiuyu, Zhang Dingshan, Wang Raoqiong, Sun Shihan, Li Yuanyuan, Wan Zhenxun, Qian Yumei, Yang Xinrui, Luo Gang, Chen Mingtai, Liu Mengnan
School of Pharmacy, Southwest Medical University, Luzhou, Sichuan, P.R. China.
Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, Sichuan, P.R. China.
Sci Rep. 2025 Jul 11;15(1):25127. doi: 10.1038/s41598-025-10631-9.
Zhilong Huoxue Tongyu capsule (ZL) is wildly used as a Chinese patent medicine for the treatment of cardiovascular diseases. Clinical studies have found that it can significantly improve hypertension and heart failure. However, its precise molecular mechanisms remain incompletely understood. The aim of this study was to investigate the effect of ZL on myocardial fibrosis (MF) in in vivo and its potential mechanisms. We established a hypertensive MF model by subcutaneous pumping of angiotensin II (Ang II) into mice, and validated in vivo whether ZL can reduce systolic blood pressure (SBP) and inhibit MF, including the use of echocardiography and various pathological staining techniques. Mechanistically, Western blot, qRT-PCR, and various immunostaining techniques were used to verify whether ZL can regulate TGF-β1/Smad3/Erbb4-IR/miR-29b pathway, and in vivo overexpression of Erbb4-IR was used to clarify whether it plays a key role in this pathway. ZL significantly reduced SBP in hypertensive MF mice, improved cardiac function and MF. Deposition of various collagen, expression of inflammatory factors, and activation of TGF-β1/Smad3 pathway is inhibited due to the intervention of ZL. In addition, ZL significantly reduced expression of Erbb4-IR and increased the expression of miR-29b. Mechanistically, after overexpression of Erbb4-IR in vivo, the regulatory effect of ZL on TGF-β1/Smad3/Erbb4-IR/miR-29b was reversed. Our results initially demonstrated ZL could exert cardioprotective effects in hypertensive MF mice. The pharmacological mechanism of ZL may be related to its regulation on TGF-β1/Smad3/Erbb4-IR/miR-29b pathway.
芪龙活血通瘀胶囊(ZL)作为一种治疗心血管疾病的中成药被广泛应用。临床研究发现,它能显著改善高血压和心力衰竭。然而,其确切的分子机制仍未完全明确。本研究旨在探讨ZL对体内心肌纤维化(MF)的影响及其潜在机制。我们通过向小鼠皮下注射血管紧张素II(Ang II)建立高血压MF模型,并在体内验证ZL是否能降低收缩压(SBP)并抑制MF,包括使用超声心动图和各种病理染色技术。从机制上讲,采用蛋白质免疫印迹法、定量逆转录聚合酶链反应(qRT-PCR)和各种免疫染色技术来验证ZL是否能调节转化生长因子-β1(TGF-β1)/Smad3/表皮生长因子受体4-胰岛素受体(Erbb4-IR)/微小RNA-29b(miR-29b)通路,并通过体内过表达Erbb4-IR来阐明其是否在该通路中起关键作用。ZL显著降低了高血压MF小鼠的SBP,改善了心脏功能和MF。由于ZL的干预,各种胶原蛋白的沉积、炎症因子的表达以及TGF-β1/Smad3通路的激活均受到抑制。此外,ZL显著降低了Erbb4-IR的表达并增加了miR-29b的表达。从机制上讲,在体内过表达Erbb4-IR后,ZL对TGF-β1/Smad3/Erbb4-IR/miR-29b的调节作用被逆转。我们的结果初步表明,ZL可在高血压MF小鼠中发挥心脏保护作用。ZL的药理机制可能与其对TGF-β1/Smad3/Erbb4-IR/miR-29b通路的调节有关。