Effect Of Extract Of Ginkgo Biloba(EGb) On Cell Of Neonatal Rat Cardiocyte Hypertrophy Induced By Prostaglandin F2 Alpha

Background:Cardiocyte hypertrophy plays an important role in cardiovascular diseases. Thus, Inhibition of this process could be a novel target for therapy in clinical treatment. Many factors can stimulate cardiocyte hypertrophy. Among them, PGF2αis one of prostaglandins'product that is generated by free radical-catayzed peroxidation from arachidonic acid on cell membranes. The aim of the present research is to analyze the possible effect of extract of ginkgo biloba on oxygen free radicals and mechanisms of cardiocyte hypertrophy induced by prostaglandin F2 alpha. In order to find a new valuable way of drug prevention and treatment of cardiocyte hypertrophy by means of oxygen free radicals as a target.Objective:Neonatal rat ventricular myocytes cultures were prepared. We observed and compared the effect of prostaglandin F2 alpha and extract of ginkgo biloba(EGb) on the cell surface , the level of intracellular ROS and the total protein of cells of cardiocyte hypertrophy. In order to investigate the effects and potential mechanisms of extract of ginkgo biloba(EGb) on the cell of cardiocyte hypertrophy induced by prostaglandin F2 alpha.Methods:Normal cells were used as negative control, and spontaneously PGF2αand EGb were used as experimental groups in this study. The cells were isolated and cultured on cultured neonatal rat cardiocyte by PGF2α, cardiocyte hypertrophy was determined by the cell surface and the total protein of cells; the level of intracellular ROS measured by the fluorescence microscope.Results:In cardiocyte hypertrophy, the cell surface , the level of intracellular ROS and the total protein of cells increased significantly in cutured neonatal rat cardiac treated with PGF2a, PGF2a causes a dose-dependent irratation of cardiocyte hypertrophy. Compared with cells treated with PGF2α, EGb(40μg/ml, 80μg/ml, 100μg/ml) inhibited cardiocyte hypertrophy by PGF2α-induced, decreased in the cell surface by 19%,27%,33% and in the total protein of cells by 21%,39%,47%, respectively (all P <0.01) , and in the fluoreacence intensity of intracellular DCF-DA by 21%,39%,47%(P <0.01).Conclusion:Prostaglandin F2αis shown to stimulate hypertrophy of neonatal rat ventricular myocytes, and EGb could suppress cardiocyte hypertrophy induced by PGF2αin the study. It indicates that the effect of EGb on cardiocyte hypertrophy induced by PGF2αcould be concerned with the suppression of intracellular ROS activity.Based on above, activation of generation of reactive oxygen species increase in cardiocyte hypertrophy, and the results of our research suggest that oxygen free radicals might play key roles in cardiocyte hypertrophy induced by PGF2αAdvanced study should be done on using reactive oxygen species as a target to provide clinic possible new therapeutic methods. EGb can inhibit cardiocyte hypertrophy by decreasing in activation of reactive oxygen species. This research has great importance in investigating pathogenesis of cardiocyte hypertrophy, synthesizing new specific drugs for prevention and treatment of cardiocyte hypertrophy into the clinical setting.