2. Academic Validation
  3. Salidroside attenuates myocardial remodeling in DOCA-salt-induced mice by inhibiting the endothelin 1 and PI3K/AKT/NFκB signaling pathways

Salidroside attenuates myocardial remodeling in DOCA-salt-induced mice by inhibiting the endothelin 1 and PI3K/AKT/NFκB signaling pathways

  • Eur J Pharmacol. 2023 Dec 2:176236. doi: 10.1016/j.ejphar.2023.176236.
Qiao Liu 1,  Qingman Luo 2,  Bin Zhong 3,  Kecheng Tang 4,  XueLing Chen 5,  Shengqian Yang 6,  Xiaohui Li 7
Affiliations

Affiliations

  • 1 Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Army Medical University, Chongqing, 400038, China; Department of Pharmaceutical, Chongqing Medical and Pharmaceutical College, Chongqing, 401331, China. Electronic address: lqiao1023@163.com.
  • 2 Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Army Medical University, Chongqing, 400038, China. Electronic address: qmlll567@163.com.
  • 3 Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Army Medical University, Chongqing, 400038, China. Electronic address: a7726785@163.com.
  • 4 Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Army Medical University, Chongqing, 400038, China. Electronic address: tkc958766833@163.com.
  • 5 Chongqing School of Pharmacy and Bioengineering, Chongqing University of Technology, Chongqing, 400054, China. Electronic address: 594528903@qq.com.
  • 6 Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Army Medical University, Chongqing, 400038, China. Electronic address: saintchyang@163.com.
  • 7 Institute of Materia Medica and Department of Pharmaceutics, College of Pharmacy, Army Medical University, Chongqing, 400038, China. Electronic address: lpsh008@aliyun.com.
PMID: 38048979 DOI: 10.1016/j.ejphar.2023.176236
Abstract

Myocardial remodeling, which occurs in the final stage of cardiovascular diseases such as hypertension, can ultimately result in heart failure. However, the pathogenesis of myocardial remodeling remains incompletely understood, and there is currently a lack of safe and effective treatment options. Salidroside, which is extracted from the plant Rhodiola rosea, shows remarkable antioxidant and anti-inflammatory characteristics. The purpose of this investigation was to examine the cardioprotective effect of salidroside on myocardial remodeling, and clarify the associated mechanism. Salidroside effectively attenuated cardiac dysfunction, myocardial hypertrophy, myocardial fibrosis, and cardiac inflammation, as well as renal injury and renal fibrosis in an animal model of deoxycortone acetate (DOCA)-salt-induced myocardial remodeling. The cardioprotective effect of salidroside was mediated by inhibiting the endothelin 1 and PI3K/Akt/NFκB signaling pathways. Salidroside was shown to inhibit the expression of endothelin1 in the hearts of mice treated with DOCA-salt. Additionally, it could prevent cardiomyocyte hypertrophy induced by endothelin-1 stimulation. Furthermore, Salidroside could effectively inhibit the excessive activation of the PI3K/Akt/NFκB pathway, which was caused by DOCA-salt treatment in mouse hearts and endothelin 1 stimulation in cardiomyocytes. Our study suggests that salidroside can be used as a therapeutic agent for the treatment of myocardial remodeling.

Keywords

Endothelin-1; Myocardial remodeling; PI3K/AKT/NFκB; Salidroside.

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