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Vanillic Acid Alleviates Acute Myocardial Hypoxia/Reoxygenation Injury by Inhibiting Oxidative Stress.
Yao, Xiuya; Jiao, Shoufeng; Qin, Mingming; Hu, Wenfeng; Yi, Bo; Liu, Dan.
Afiliación
  • Yao X; Jiangxi Provincial Key Laboratory of Basic Pharmacology, Nanchang University, School of Pharmaceutical Science, Nanchang 330006, China.
  • Jiao S; Department of Pharmacy, Changzhou Maternal and Child Health Care Hospital, Changzhou 213000, China.
  • Qin M; Department of Pharmacy, The First Affiliated Hospital of Nanchang University, Nanchang 330006, China.
  • Hu W; Jiangxi Provincial Key Laboratory of Basic Pharmacology, Nanchang University, School of Pharmaceutical Science, Nanchang 330006, China.
  • Yi B; Jiangxi Provincial Key Laboratory of Basic Pharmacology, Nanchang University, School of Pharmaceutical Science, Nanchang 330006, China.
  • Liu D; Second Abdominal Surgery Department, Jiangxi Province Tumor Hospital, Nanchang 330029, China.
Oxid Med Cell Longev ; 2020: 8348035, 2020.
Article en En | MEDLINE | ID: mdl-32377308
ABSTRACT
Oxidative stress is an important factor of myocardial hypoxia/reoxygenation (H/R) injury. Our research focuses on how to reduce the cardiac toxicity caused by oxidative stress through natural plant extracts. Vanillic acid (VA) is a phenolic compound found in edible plants and rich in the roots of Angelica sinensis. Experimental studies have provided evidence for this compound's effectiveness in cardiovascular diseases; however, its mechanism is still unclear. In this study, molecular mechanisms related to the protective effects of VA were investigated in H9c2 cells in the context of H/R injury. The results showed that pretreatment with VA significantly increased cell viability and decreased the percentage of apoptotic cells, as well as lactate dehydrogenase and creatine phosphokinase activity, in the supernatant, accompanied by reduced levels of reactive oxygen species and reduced caspase-3 activity. VA pretreatment also restored mitochondrial membrane potentials. Moreover, preincubation with VA significantly attenuated mitochondrial permeability transition pore activity. VA administration upregulated adenosine monophosphate-activated protein kinase α2 (AMPKα2) protein expression, and interestingly, pretreatment with AMPKα2-siRNA lentivirus effectively attenuated the cardioprotective effects of VA in response to H/R injury.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Ácido Vanílico / Daño por Reperfusión Miocárdica / Hipoxia de la Célula Límite: Animals / Humans Idioma: En Revista: Oxid Med Cell Longev Asunto de la revista: METABOLISMO Año: 2020 Tipo del documento: Article País de afiliación: China

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Ácido Vanílico / Daño por Reperfusión Miocárdica / Hipoxia de la Célula Límite: Animals / Humans Idioma: En Revista: Oxid Med Cell Longev Asunto de la revista: METABOLISMO Año: 2020 Tipo del documento: Article País de afiliación: China
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