Apocynin prevents isoproterenol-induced cardiac hypertrophy in rat
Autor: | Nikhat Saleem, Shyamal K. Goswami, Anamika Prasad |
---|---|
Rok vydání: | 2017 |
Předmět: |
Male
0301 basic medicine Clinical Biochemistry Adrenergic 030204 cardiovascular system & hematology medicine.disease_cause Muscle hypertrophy Pathogenesis chemistry.chemical_compound 0302 clinical medicine chemistry.chemical_classification NADPH oxidase biology Heart Organ Size General Medicine Adrenergic beta-Agonists Glutathione Up-Regulation Echocardiography NADPH Oxidase 2 Oxidation-Reduction Signal Transduction medicine.medical_specialty Cardiomegaly 03 medical and health sciences Internal medicine medicine Animals RNA Messenger Rats Wistar Molecular Biology Reactive oxygen species business.industry Body Weight Isoproterenol Acetophenones NADPH Oxidases Cell Biology Enzyme Activation Oxidative Stress 030104 developmental biology Endocrinology chemistry Apocynin biology.protein Reactive Oxygen Species business Protein Kinases Biomarkers Oxidative stress |
Zdroj: | Molecular and Cellular Biochemistry. 445:79-88 |
ISSN: | 1573-4919 0300-8177 |
Popis: | Oxidative stress is implicated in the pathogenesis of a plethora of cardiovascular diseases including interstitial fibrosis, contractile dysfunction, ischemia-reperfusion injury, and cardiac remodeling. However, antioxidant therapies targeting oxidative stress in the progression of those diseases have largely been unsuccessful. The current study evaluated the effects of a NADPH oxidase inhibitor, apocynin (Apo), on the production of reactive oxygen species and the development of pathological cardiac hypertrophy under sustained β-adrenergic stimulation in male Wistar rats. As evident from the HW/BW ratio, HW/TL ratio, echocardiography, and histopathology, hypertrophic responses induced by isoproterenol (Iso; 5 mg/Kg body weight, subcutaneous) were blocked by Apo (10 mg/Kg body weight, intraperitoneal). Iso treatment increased the transcript levels of cybb and p22-phox, the two subunits of Nox. Iso treatment also caused a decrease in reduced glutathione level that was restored by Apo. Increase in mRNA levels of a number of markers of hypertrophy, viz., ANP, BNP, β-MHC, and ACTA-1 by Iso was either partially or completely prevented by Apo. Activation of key signaling kinases such as PKA, Erk, and Akt by Iso was also prevented by Apo treatment. Our study thus provided hemodynamic, biochemical, and molecular evidences supporting the therapeutic value of Apo in ameliorating adrenergic stress-induced cardiac hypertrophy. |
Databáze: | OpenAIRE |
Externí odkaz: |