ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Cardiovascular and Smooth Muscle Pharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1604408
Gastrodin reduces myocardial ischemia/reperfusion injury via Transgelin2/CNPase-mediated apoptosis regulation
Provisionally accepted
Changyan Li1Peng Rao1
Xiang Liu2Lin Yang3Yongliang Jiang1Gaosheng Yin1Shuangxiu Li3Ping Yang3
Sun Lin3*- 1Kunming Medical University, Kunming, Yunnan Province, China
- 2The First People’s Hospital of Yunnan Province, Kunming, Yunnan Province, China
- 3The Second Affiliated Hospital of Kunming Medical University, Kunming, China
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Abstract： BACKGROUND: Myocardial ischemia-reperfusion injury (MIRI) frequently occurs during rapid restoration of blood flow in the infarcted myocardium. While Gastrodin (GAS) mitigates MIRI, its mechanism requires further exploration. METHODS: We evaluated GAS effect in SD rats following 45-min left coronary artery ligation and reperfusion. GAS (intraperitoneal) was administered preoperatively for 3 days. Triphenyltetrazolium chloride (TTC) staining was used to detect infarct size. The cardiac function was monitored by the Langendorff isolated cardiac perfusion system. Hematoxylin-Eosin (H&E) staining was applied to detect cardiac injury. H9c2 cells underwent oxygen and glucose deprivation (OGD) and were subsequently restored to normal culture conditions, mimicking MIRI. Cell Counting Kit-8 (CCK-8) was used to detect the cytotoxicity of GAS. Myocardial cell injury was determined by detecting lactate dehydrogenase (LDH) level in the medium. The expression of protein was detected by western blot (WB) and immunofluorescence (IF) assay. Coimmunocoprecipitation (Co-IP), coupled with molecular docking detected the combination among transgelin2 (TG2), and CNPase. RESULTS: GAS reduced the size of myocardial infarction, alleviated myocardial fiber damage, and ameliorated MIRI-mediated cardiac dysfunction. Mechanistically, GAS inhibited apoptosis by restoring MIRI-altered TG2/CNPase expression. TG2 directly bound and negatively regulated CNPase. CNPase deficiency enhanced MIRI amelioration by reducing apoptosis. CONCLUSIONS: Taken together, GAS protects against MIRI by modulating apoptosis through the TG2/CNPase pathway, revealing a novel therapeutic target.
Keywords: Myocardial ischemia/reperfusion injury, Gastrodin, Apoptosis, CNPase, transgelin2 1. Introduction
Received: 01 Apr 2025; Accepted: 27 Jun 2025.
Copyright: © 2025 Li, Rao, Liu, Yang, Jiang, Yin, Li, Yang and Lin. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Sun Lin, The Second Affiliated Hospital of Kunming Medical University, Kunming, China
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