Monday, September 21st, 2020


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Effect of Rutin on Angiotensin II–Induced Cardiomyocyte Hypertrophy and the Inherent Mechanism
Authors:  Liang Wang, M.M., Xuebai Lv, M.M., and Chunmei Ma, M.D.
  Objective: To establish a cardiomyocyte hypertrophy model, observe the effects of rutin on hypertrophic cardiomyocytes, and explore the possible mechanism. METHODS: Cardiomyocytes of neonatal rats were cultured in vitro. The survival rate of cardiomyocytes was observed by CCK-8 method. The surface area of myocardial cells and the concentration of intracellular calcium ions were detected by laser confocal microscopy. The activity of Ca2+ ATPase was determined by the enzymatic reaction of broken cells. The expressions of Ca MKII, HDAC, c-Jun, ANP, BNP, β-MHC, Ca N, and NFAT-3 proteins were detected by western blot. The concentration of nitric oxide (NO) and the activity of NOS were determined by colorimetry.
Different concentrations of rutin could inhibit the decrease of survival rate of cardiomyocytes induced by Angiotensin II (Ang II), the increase of the surface area, the increase of the Ca2+ concentration in cardiomyocytes, and the decrease of the activity of Ca2+ ATPase, the increment of the relative expressions of Ca MKII, HDAC, Ca N, and NFAT-3 proteins, and the increase of the relative expressions of c-Jun, ANP, BNP, and β-MHC proteins. The decrease in NO concentration and NOS activity also has been inhibited to a certain degree.
Rutin has significant inhibitory and protective effects on Ang II–induced hypertrophic cardiomyocytes, and the mechanism may be related with the release of NO, the regulation of intracellular Ca2+ concentration and Ca2+ ATPase activity, as well as the block of calcium ion-mediated Ca N-NFAT-3 and the Ca MK II-HDAC signal transduction pathways.
Keywords:  angiotensin II, cardiac hypertrophy, cardiomyocyte hypertrophy, cisplatin toxicity, heart, heart/drug effects, heart/physiopathology, nitric oxide, rutin
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