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目的探讨N-乙酰基—丝氨酰—天门冬酰—赖氨酰—脯氨酸(AcSDKP)抗心肌纤维化的可能机制。方法将大鼠心脏成纤维细胞随机分为三组,对照组予0.4%胎牛血清的DMEM;转化生长因子(TGF)-β1组在0.4%胎牛血清的DMEM中加入终质量浓度为5 ng/ml的TGF-β1;AcSDKP组在5 ng/ml的TGF-β1诱导刺激同时加入终质量浓度为10-9mol/L的AcSDKP。Western blot法检测MMP-1、TIMP-1、Ⅰ和Ⅲ型胶原表达。结果 TGF-β1可使MMP-1表达下降,TIMP-1表达升高,MMP-1/TIMP-1值下降;AcSDKP抑制TGF-β1对MMP-1的作用,使MMP-1表达增加,但对TIMP-1表达无明显影响,MMP-1/TIMP-1值增加。同时AcSDKP减弱由TGF-β1诱导的Ⅰ和Ⅲ型胶原表达,并降低Ⅰ/Ⅲ型值。结论 AcSDKP抗纤维化的作用机制可能是调节胶原合成/降解代谢的平衡,加速细胞外基质降解,同时抑制Ⅰ和Ⅲ型胶原生成。
Objective To investigate the possible mechanism of anti-myocardial fibrosis of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP). Methods Rat cardiac fibroblasts were randomly divided into three groups, the control group was given 0.4% fetal bovine serum DMEM; TGF-β1 group in 0.4% fetal bovine serum DMEM final concentration of 5 ng / ml of TGF-β1; AcSDKP group in 5 ng / ml TGF-β1-induced stimulation while adding the final concentration of 10-9mol / L of AcSDKP. Western blot was used to detect the expression of MMP-1, TIMP-1, type I and type III collagen. Results TGF-β1 could decrease the expression of MMP-1, increase the expression of TIMP-1 and decrease the expression of MMP-1 / TIMP-1. AcSDKP inhibited the effect of TGF-β1 on MMP-1 and increased the expression of MMP- TIMP-1 expression had no significant effect, MMP-1 / TIMP-1 increased. At the same time, AcSDKP attenuated the expression of type I and type III collagen induced by TGF-β1 and decreased the type I / III. Conclusion The anti-fibrosis mechanism of AcSDKP may be to regulate the balance of collagen synthesis / metabolism, accelerate the degradation of extracellular matrix, and inhibit the formation of type I and type III collagen.