2. Academic Validation
  3. Gastrodin alleviates myocardial infarction by inhibiting inflammation, and apoptosis and promoting endothelial cell proliferation

Gastrodin alleviates myocardial infarction by inhibiting inflammation, and apoptosis and promoting endothelial cell proliferation

  • Biochem Biophys Rep. 2025 Apr 18:42:102014. doi: 10.1016/j.bbrep.2025.102014.
Ruochen Du 1,  Ying Guo 2,  Wanting Zhong 3,  Yuantao Gao 4,  Miaomiao Xu 3,  Chunfang Wang 1 2,  Yitong Yuan 1 2
Affiliations

Affiliations

  • 1 Department of Laboratory Animal Center, Shanxi Medical University, Taiyuan, 030001, Shanxi, People's Republic of China.
  • 2 College of Basic Medical, Shanxi Medical University, Taiyuan, 030001, Shanxi, People's Republic of China.
  • 3 Academy of Medical Sciences, Shanxi Medical University, Taiyuan, 030001, Shanxi, People's Republic of China.
  • 4 Department of Otorhinolaryngology-Head and Neck Surgery, The Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, 310052, People's Republic of China.
PMID: 40290804 DOI: 10.1016/j.bbrep.2025.102014
Abstract

Gastrodin, a bioactive ingredient extracted from the Chinese herb Gastrodia gastrodia, has shown potential therapeutic effects in cardiovascular diseases, but its specific role in myocardial infarction is unclear. This study investigated the protective effect of gastrodin on myocardial infarction and its potential mechanism. By clamping the left coronary artery, we created a model of myocardial infarction in C57BL/6J mice. For 14 days, mice in the control and myocardial infarction groups received a daily dose of 100 mg/kg gastrodin. Gastrodin significantly improved cardiac dysfunction in mice with myocardial infarction, decreased heart weight/body weight (HW/BW) and heart weight/tibial length (HW/TL) ratios, and inhibited mRNA expression levels of cardiac fibrosis biomarkers (Collagen Type I (Col1), Collagen Type III (Col3), Matrix Metalloproteinase-2 (MMP-2), Matrix Metalloproteinase-9 (MMP-9)). In addition, gastrodin also inhibited the activity of Apoptosis marker Caspase 3, decreased the Bax/Bcl2 mRNA ratio, decreased the expression of pro-inflammatory factors (Interleukin-1 beta (IL-1β), Tumor Necrosis Factor-alpha (TNF-α), Interleukin-6 (IL-6)) and pro-inflammatory adhesion molecule Monocyte Chemoattractant Protein-1 (MCP1), and promoted the expression of angiogenesis marker Cluster of Differentiation 31 (CD31). RNA Sequencing and Rt-qPCR analysis showed that gastrodin treatment significantly up-regulated the expression of genes related to cell proliferation (Cyclin-Dependent Kinase 1 (CDK1), Threonine Tyrosine Kinase (TTK), Cyclin B2 (CCNB2), Polo-Like Kinase 1 (PLK1)), and promoted the proliferation of human aortic endothelial cells (HAECs). These findings suggest that gastrodin can effectively reduce the pathological changes of myocardial infarction by inhibiting inflammation, reducing Apoptosis, and promoting endothelial cell proliferation, thus providing a new strategy for the prevention and treatment of myocardial infarction.

Keywords

Angiogenesis; Apoptosis; Endothelial proliferation; GAS; Inflammation; Myocardial infarction.

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