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Forskolin Protected against Streptozotocin-Induced Diabetic Cardiomyopathy via Inhibition of Oxidative Stress and Cardiac Fibrosis in Mice.
Zhang, Xu; Ke, Pei-Xiong; Yuan, Xun; Zhang, Gui-Ping; Chen, Wen-Liang; Zhang, Gen-Shui.
Afiliación
  • Zhang X; Key Laboratory of Molecular Clinical Pharmacology & Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, Guangdong 511436, China.
  • Ke PX; Key Laboratory of Molecular Clinical Pharmacology & Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, Guangdong 511436, China.
  • Yuan X; Key Laboratory of Molecular Clinical Pharmacology & Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, Guangdong 511436, China.
  • Zhang GP; Key Laboratory of Molecular Clinical Pharmacology & Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, Guangdong 511436, China.
  • Chen WL; Department of Biology, York University, 4700 Keele Street, Toronto, ON, Canada M3J 1P3.
  • Zhang GS; Key Laboratory of Molecular Clinical Pharmacology & Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, Guangdong 511436, China.
Biomed Res Int ; 2021: 8881843, 2021.
Article en En | MEDLINE | ID: mdl-33564685
BACKGROUND: Diabetic cardiomyopathy is one of the cardiac complications in diabetes patients, eventually resulting in heart failure and increasing morbidity and mortality. Oxidative stress is a critical pathological feature in diabetic hearts, contributing to the development of DCM. Forskolin (FSK) was shown to reduce oxidative stress. This study was aimed at investigating the effects of FSK on diabetic hearts and the relevant molecular mechanisms. METHODS: Streptozotocin- (STZ-) induced diabetes in mice was treated with FSK through intraperitoneal injection. Cardiac functions were evaluated by echocardiography. Hematoxylin-eosin and Masson trichrome staining was employed to determine heart morphological changes and cardiac fibrosis, respectively. Cardiac fibrosis-related markers were detected by western blot. Superoxide dismutase activity, reduced/oxidized glutathione ratio, and malondialdehyde concentration in left ventricles were determined using respective commercial kits. RESULTS: Abnormal cardiac diastolic dysfunction and cardiac fibrosis were observed in diabetic hearts. FSK treatment significantly improved the cardiac diastolic function and attenuated the abnormal morphological change in diabetic hearts. Moreover, FSK treatment in diabetic mice decreased the expression of fibronectin, collagen I, TGF-ß, and α-SMA and reduced myocardial fibrosis. Furthermore, we observed that FSK significantly blocked oxidative stress in diabetic hearts. CONCLUSIONS: Our study demonstrates that FSK protects against the development of DCM in STZ-induced diabetes in mice. Our study suggests that FSK might be a potential target for drug development in treating DCM.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Colforsina / Estrés Oxidativo / Diabetes Mellitus Experimental / Cardiomiopatías Diabéticas Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Biomed Res Int Año: 2021 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Colforsina / Estrés Oxidativo / Diabetes Mellitus Experimental / Cardiomiopatías Diabéticas Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Biomed Res Int Año: 2021 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos