AcSDKP对PDGF诱导的大鼠心脏成纤维细胞增殖和胶原合成的调节作用

目的：探讨N-乙酰基-丝氨酰-天门冬酰-赖氨酰-脯氨酰（AcSDKP）对血小板源性生长因子（PDGF）诱导的大鼠心脏成纤维细胞增殖和胶原合成的调节作用。方法：建立新生大鼠心脏成纤维细胞系;采用四甲基偶氮唑（MTT）法和^3H-TdR掺入法检测心脏成纤维细胞的增殖;采用^3H-脯氨酸掺入法检测心脏成纤维细胞胶原的合成。结果：PD3F在1～20ng／ml浓度范围内对心脏成纤维细胞增殖和胶原合成均有促进作用。且随着PDGF浓度的增加,其促细胞增殖和胶原合成作用增强,并在10ng／ml浓度时PDGF的促增殖和胶原合成效应最强。在10^-10～10^-8mol／L浓度范围内,AcSDKP对PDGF介导的心脏成纤维细胞增殖和胶原合成均有抑制作用,并且在10叫mol／L时,AcSDKP抑制心脏成纤维细胞增殖和胶原合成作用最强。结论：AcSDKP对PDGF介导的心脏成纤维增殖和胶原合成均有明显抑制作用,这可能与其抗心脏纤维化的作用相关。

Effect of AcSDKP on the proliferation and collagen synthesis in cultured rat cardiac fibroblasts stimulated by PDGF

Aim: To investigate whether AcSDKP can inhibit proliferation and collagen synthesis in cultured rat cardiac fibroblasts mediated by PDGF.Methods: Neonatal rat cardiac fibroblasts were isolated.The cell proliferation was observed by 3H-proline incorporation assay.Results: On the culture of 0.4% FBS,PDGF stimulated cardiac fibroblasts proliferation and collagen synthesis with a dose-dependent manner at the concentrations from 1 ng/ml to 20 ng/ml,in which 10 ng/ml PDGF reached its peak.AcSDKP at the concentration from 10-10mol/L to 10-8mol/L could inhibit cardiac fibroblasts proliferation and collagen synthesis mediated by PDGF.10-9mol/L AcSDKP attained its peak on inhibiting cardiac fibroblasts proliferation and collagen synthesis.Conclusion: AcSDKP can inhibit proliferation and collagen synthesis in cultured rat cardiac fibroblasts mediated by PDGF.