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 |
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| Otros Autores: | , , , , , , , |
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| 003 | UK-CbPIL | ||
| 022 | |a 1663-9812 | ||
| 024 | 7 | |a 1604408 |2 doi | |
| 035 | |a 3279098205 | ||
| 045 | 2 | |b d20250701 |b d20250731 | |
| 100 | 1 | |a Li, Changyan |u Yunnan Key Laboratory of Stem Cell and Regenerative Medicine, School of Rehabilitation, Kunming Medical University, Kunming, China | |
| 245 | 1 | |a Gastrodin reduces myocardial ischemia/reperfusion injury via transgelin2/CNPase-mediated apoptosis regulation | |
| 260 | |b Frontiers Media SA |c Jul 2025 | ||
| 513 | |a Journal Article | ||
| 520 | 3 | |a 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. | |
| 653 | |a Cytotoxicity | ||
| 653 | |a Blood flow | ||
| 653 | |a Mortality | ||
| 653 | |a Cell culture | ||
| 653 | |a Therapeutic targets | ||
| 653 | |a Cell injury | ||
| 653 | |a Pericardium | ||
| 653 | |a Electrocardiography | ||
| 653 | |a Congenital diseases | ||
| 653 | |a Myocardial infarction | ||
| 653 | |a Apoptosis | ||
| 653 | |a L-Lactate dehydrogenase | ||
| 653 | |a Reperfusion | ||
| 653 | |a Myocardium | ||
| 653 | |a Laboratory animals | ||
| 653 | |a Coronary artery | ||
| 653 | |a Medical prognosis | ||
| 653 | |a Myocardial ischemia | ||
| 653 | |a Triphenyltetrazolium chloride | ||
| 653 | |a Immunofluorescence | ||
| 653 | |a Coronary vessels | ||
| 653 | |a Medical research | ||
| 653 | |a Cardiovascular disease | ||
| 653 | |a Veins & arteries | ||
| 653 | |a Glucose | ||
| 653 | |a Heart | ||
| 653 | |a Ischemia | ||
| 653 | |a Pulmonary hypertension | ||
| 653 | |a Cholecystokinin | ||
| 700 | 1 | |a Rao, Peng |u Yunnan Key Laboratory of Stem Cell and Regenerative Medicine, School of Rehabilitation, Kunming Medical University, Kunming, China | |
| 700 | 1 | |a Liu, Xiang |u Yunnan Key Laboratory of Stem Cell and Regenerative Medicine, School of Rehabilitation, Kunming Medical University, Kunming, China, Department of Orthopedic Surgery, The First People’s Hospital of Yunnan Province, Kunming, China | |
| 700 | 1 | |a Yang, Lin |u Yunnan Key Laboratory of Stem Cell and Regenerative Medicine, School of Rehabilitation, Kunming Medical University, Kunming, China, Department of Cardiology, the Second Affiliated Hospital, Kunming Medical University, Kunming, China | |
| 700 | 1 | |a Jiang, Yongliang |u Yunnan Key Laboratory of Stem Cell and Regenerative Medicine, School of Rehabilitation, Kunming Medical University, Kunming, China, Department of Cardiology, the Second Affiliated Hospital, Kunming Medical University, Kunming, China | |
| 700 | 1 | |a Yin, Gaosheng |u Yunnan Key Laboratory of Stem Cell and Regenerative Medicine, School of Rehabilitation, Kunming Medical University, Kunming, China | |
| 700 | 1 | |a Li, Shuangxiu |u Yunnan Key Laboratory of Stem Cell and Regenerative Medicine, School of Rehabilitation, Kunming Medical University, Kunming, China, Department of Cardiology, the Second Affiliated Hospital, Kunming Medical University, Kunming, China | |
| 700 | 1 | |a Yang, Ping |u Yunnan Key Laboratory of Stem Cell and Regenerative Medicine, School of Rehabilitation, Kunming Medical University, Kunming, China, Department of Cardiology, the Second Affiliated Hospital, Kunming Medical University, Kunming, China | |
| 700 | 1 | |a Sun, Lin |u Department of Cardiology, the Second Affiliated Hospital, Kunming Medical University, Kunming, China | |
| 773 | 0 | |t Frontiers in Pharmacology |g vol. 16 (Jul 2025), p. 1604408-1604425 | |
| 786 | 0 | |d ProQuest |t Biological Science Database | |
| 856 | 4 | 1 | |3 Citation/Abstract |u https://www.proquest.com/docview/3279098205/abstract/embedded/7BTGNMKEMPT1V9Z2?source=fedsrch |
| 856 | 4 | 0 | |3 Full Text |u https://www.proquest.com/docview/3279098205/fulltext/embedded/7BTGNMKEMPT1V9Z2?source=fedsrch |
| 856 | 4 | 0 | |3 Full Text - PDF |u https://www.proquest.com/docview/3279098205/fulltextPDF/embedded/7BTGNMKEMPT1V9Z2?source=fedsrch |