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
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