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Updated: May 22, 2026
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Liqi Huatan Huoxue Formula Rescued Myocardial Cell Apoptosis of Coronary Microvascular Dysfunction Rat by Inhibiting
Zhao Ge1,2, Qiuan Ren3, Xianliang Wang1,2
1First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Background:
Coronary microvascular dysfunction (CMD) is a critical pathological condition linked to impaired myocardial perfusion and poor cardiovascular outcomes.
Objectives:
This study aimed to establish a CMD rat model and evaluate the therapeutic effects of the traditional Chinese medicine formula Liqi Huatan Huoxue (LQHTHX), with a focus on apoptosis, oxidative stress, and vascular endothelial function.
Materials And Methods:
CMD was induced in rats via intraventricular injection of sodium laurate (1 mL/kg, 1 g/L). The therapeutic efficacy of LQHTHX was assessed using hematoxylin-eosin (HE) and Masson staining, ELISA, biochemical assays, and TUNEL apoptosis assays. Western blotting (WB) and qRT-PCR were employed to evaluate the regulatory effects of LQHTHX on the NRG-1/ErbB signaling pathway and its downstream mitochondrial and endoplasmic reticulum (ER) stress pathways.
Results:
LQHTHX treatment improved microvascular structure and reduced thrombus obstruction in CMD rats. It enhanced antioxidant capacity, restored vascular endothelial balance, and significantly reduced cardiomyocyte apoptosis. LQHTHX modulated the NRG-1/ErbB pathway and decreased the expression of pro-apoptotic proteins (Bax, Bad, Cyt-c, and Caspase-3), while increasing Bcl-2 levels. Furthermore, it suppressed ER stress-related apoptotic markers (CHOP, GRP78, and Caspase-12).
Conclusions:
LQHTHX ameliorates CMD by inhibiting apoptosis through mitochondrial and ER stress pathways, enhancing antioxidant defenses, and protecting vascular endothelial function.
