Effects Of Schisandrin B On Angiotensin Ⅱ Inducecd Cardiac Fibroblasts Proliferation

Objective:.To study the effects of Connexin 43,TGF-β and AKT on the proliferation of cardiac fibroblasts induced by angiotensin Ⅱ and the effect of schisandrin B on the proliferation of cardiac fibroblasts induced by angiotensin Ⅱ.Methods:1-3 day SD rat heart was used in this study and hearts were digested with 0.1%collagenase digestion,then using the differential adherence method to isolated cultured cardiac fibroblasts.MTT proliferation method was used to determine the angiotensin Ⅱ concentration which can better enhance cardiac fibroblast proliferation.Western blot method was used to investigate connexin 43,TGF-β and AKT protein expression by angiotensin Ⅱ and Schisandrin B drug intervention.Results:1.MTT experimental results showed that Ang Ⅱ induce cardiac fibroblast proliferation,and the concentration of 10-7 mol·L-1 is most obvious and with statistical significance(P<0.05)and Ang Ⅱ 10-7mol·L-1 24 h group growth rate has significant difference compared to 12 h and 36 h growth rate(P<0.01).2.According to the TGF-P antibody band analysis,Ang Ⅱ 10-6mol·L-1、10-7mol·L-1 group significantly increased the protein expression compared with the control group(P<0.01);the protein expression was significantly inhibited by schisandrin B 100 μmol/L 24 h intervention(P<0.05);Ang Ⅱ 10-6 mol·L-1、10-7 mol·L-1 group significantly increased AKT protein compared with the control group(P<0.01);but after schisandrin B 100μmol/L 24 h intervention,AKT protein expression were significantly decreased(P<0.05);Connexin 43 protein expression was significantly enhanced by Ang Ⅱ 10-6 mol·L-1 1 h,2 h t:reatment compared with the blank group(P<0.01),losartan potassium treatment for 30 min and L-NAME treatment for 30 min were significantly decreased connexin 43 level induced by Ang Ⅱ 10-6 mol·L-1(P<0.05).Conclusion:1.Ang Ⅱ induces proliferation of cardiac fibroblasts by enhancing the expression of TGF-β,AKT and Connexin 43 protein.2.The effect of schisandrin B on TGF-β and AKT protein expression can inhibit the proliferation of cardiac fibroblasts induced by Ang Ⅱ.