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Gastrodin reduces myocardial ischemia/reperfusion injury via transgelin2/CNPase-mediated apoptosis regulation

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Publicado en:Frontiers in Pharmacology vol. 16 (Jul 2025), p. 1604408-1604425
Autor Principal: Li, Changyan
Outros autores: Rao, Peng, Liu, Xiang, Yang, Lin, Jiang, Yongliang, Yin, Gaosheng, Li, Shuangxiu, Yang, Ping, Sun, Lin
Publicado:
Frontiers Media SA
Materias:
Cytotoxicity
Blood flow
Mortality
Cell culture
Therapeutic targets
Cell injury
Pericardium
Electrocardiography
Congenital diseases
Myocardial infarction
Apoptosis
L-Lactate dehydrogenase
Reperfusion
Myocardium
Laboratory animals
Coronary artery
Medical prognosis
Myocardial ischemia
Triphenyltetrazolium chloride
Immunofluorescence
Coronary vessels
Medical research
Cardiovascular disease
Veins & arteries
Glucose
Heart
Ischemia
Pulmonary hypertension
Cholecystokinin
Acceso en liña:Citation/Abstract
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Resumo:BackgroundMyocardial 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.MethodsWe 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.ResultsGAS 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.ConclusionTaken together, GAS protects against MIRI by modulating apoptosis through the TG2/CNPase pathway, revealing a novel therapeutic target.
ISSN:1663-9812
DOI:1604408
Fonte:Biological Science Database