ArticleBiochemistry and biophysics reports2025
Gastrodin alleviates myocardial infarction by inhibiting inflammation, and apoptosis and promoting endothelial cell proliferation.
Article in Biochemistry and biophysics reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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