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目的研究牛磺酸(Taurine,Tau)对血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导新生大乳鼠心肌成纤维细胞(myofibroblasts,myo Fbs)增殖的抑制作用,并探讨其作用机制.方法用AngⅡ诱导新生大乳鼠myo Fbs增殖,建立心肌纤维化(myofibrosis,MF)模型.采用四甲基偶氮唑盐(MTT)法检测细胞增殖;羟脯氨酸试剂盒检测胶原含量;免疫细胞化学染色检测p-PKCα的膜转位及表达;Western blot检测p-PKCα和p-ERK1/2蛋白表达及含量.结果 Tau(30,60,120)mmol/L可明显抑制AngⅡ诱导的Myo Fbs增殖及胶原合成,同AngⅡ组比较差异具有统计学意义(P<0.05或P<0.01),并且呈现出剂量依赖性.应用免疫细胞染色Western blot并且结合图像分析,结果表明:Tau可抑制p-PKCα膜转位和表达,与AngⅡ组相比差异具有统计学意义(P<0.01).结论 Tau可能通过减少p-PKCα的表达及膜转位,从而抑制MyoFbs增殖和胶原含量的增加,抑制MF,逆转心肌重塑.
Objective To investigate the inhibitory effect of Taurine on the proliferation of myogenic fibroblasts (myo fibroblasts) induced by angiotensin Ⅱ (AngⅡ) and its mechanism of action.Methods Ang Ⅱ Myofibrils were proliferated and myofibrosis (MF) models were established.MTT assay was used to detect cell proliferation, hydroxyproline kit was used to detect collagen content, and immunocytochemical staining The protein expression and content of p-PKCα and p-ERK1 / 2 were detected by Western blot.Results Tau (30,60,120) mmol / L could significantly inhibit AngⅡ-induced Myo Fbs proliferation and collagen synthesis, Compared with AngⅡ group, the difference was statistically significant (P <0.05 or P <0.01), and showed a dose-dependent manner.Using immunocytochemistry Western blot and image analysis, the results showed that: Tau can inhibit p-PKC membrane translocation and (P <0.01) .ConclusionTau may inhibit MyoFbs proliferation and collagen content, inhibit MF and reverse myocardial remodeling by decreasing the expression of p-PKCα and membrane translocation, .