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Attenuation of ROS-mediated myocardial ischemia-reperfusion injury by morin via regulation of RISK/SAPK pathways.
Verma, Vipin Kumar; Malik, Salma; Mutneja, Ekta; Sahu, Anil Kumar; Bhatia, Jagriti; Arya, Dharamvir Singh.
Afiliación
  • Verma VK; Cardiovascular Research Laboratory, Department of Pharmacology, All India Institute of Medical Sciences, New Delhi, 110029, India.
  • Malik S; Cardiovascular Research Laboratory, Department of Pharmacology, All India Institute of Medical Sciences, New Delhi, 110029, India.
  • Mutneja E; Cardiovascular Research Laboratory, Department of Pharmacology, All India Institute of Medical Sciences, New Delhi, 110029, India.
  • Sahu AK; Cardiovascular Research Laboratory, Department of Pharmacology, All India Institute of Medical Sciences, New Delhi, 110029, India.
  • Bhatia J; Cardiovascular Research Laboratory, Department of Pharmacology, All India Institute of Medical Sciences, New Delhi, 110029, India.
  • Arya DS; Cardiovascular Research Laboratory, Department of Pharmacology, All India Institute of Medical Sciences, New Delhi, 110029, India. dsarya16@gmail.com.
Pharmacol Rep ; 72(4): 877-889, 2020 Aug.
Article en En | MEDLINE | ID: mdl-32048260
BACKGROUND: Oxidative stress plays an important role in the pathogenesis of myocardial ischemia-reperfusion (IR) injury. Morin, a bioflavonoid, has demonstrated antioxidant, anti-inflammatory and other diverse pharmacological activities in various experimental models such as isoproterenol-induced myocardial injury, doxorubicin-induced cardiotoxicity and neurotoxicity, as well as cisplatin-induced nephrotoxicity. Thus, this study aimed to evaluate the effect of morin in myocardial IR injury model and its underlying mechanisms. METHOD: To accomplish this, male albino Wistar rats were pre-treated with morin (40 and 80 mg/kg; po) for 28 days and on 29th day, rats experienced 45-min myocardial ischemia followed by 60-min reperfusion. RESULTS: In comparison to IR-control group, morin pre-treatment significantly normalized hemodynamic parameters, restored antioxidant status, improved pathological changes, reduced the release of cardiac injury markers, inhibited inflammation (TNF-α/IL-6/NFκB/IKKß) and apoptosis (increased Bcl-2, decreased Bax/Caspase-3 and TUNEL positivity) in the myocardium. This improvement in antioxidant, inflammation and anti-apoptosis markers could be due to downregulation of SAPK (p38/JNK) pathway and upregulation of survival kinase, i.e. RISK pathway (ERK/eNOS) in the myocardium. CONCLUSION: Thus, morin attenuated myocardial IR injury in rats by regulation of RISK/SAPK pathways.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Flavonoides / Daño por Reperfusión Miocárdica / Especies Reactivas de Oxígeno / Proteínas Quinasas p38 Activadas por Mitógenos / Antioxidantes Tipo de estudio: Etiology_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: Pharmacol Rep Asunto de la revista: FARMACOLOGIA Año: 2020 Tipo del documento: Article País de afiliación: India Pais de publicación: Suiza
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Flavonoides / Daño por Reperfusión Miocárdica / Especies Reactivas de Oxígeno / Proteínas Quinasas p38 Activadas por Mitógenos / Antioxidantes Tipo de estudio: Etiology_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: Pharmacol Rep Asunto de la revista: FARMACOLOGIA Año: 2020 Tipo del documento: Article País de afiliación: India Pais de publicación: Suiza