RESUMEN
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(-10) mol/L to 10(-8) mol/L could inhibit cardiac fibroblasts proliferation and collagen synthesis mediated by PDGF. 10(-9) mol/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.
Asunto(s)
Proliferación Celular , Colágeno/biosíntesis , Fibroblastos/efectos de los fármacos , Mioblastos Cardíacos/efectos de los fármacos , Oligopéptidos/farmacología , Factor de Crecimiento Derivado de Plaquetas/farmacología , Animales , Células Cultivadas , Fibroblastos/citología , Fibroblastos/metabolismo , Mioblastos Cardíacos/citología , Mioblastos Cardíacos/metabolismo , Ratas , Ratas WistarRESUMEN
OBJECTIVE: To investigate the role of AcSDKP on collagen synthesis and degradation in cultured rat cardiac fibroblasts. METHODS: Neonatal rat cardiac fibroblasts were isolated and stimulated by PDGF. The cell proliferation was observed by (3)H-TdR incorporation assay. The synthesis of collagen was measured by (3)H-proline incorporation assay. The expression of type I and type III collagen and MMP-1 protein were measured by Western blot. The MMP-2 and MMP-9 activity was evaluated with zymography assay. RESULTS: PDGF stimulated cardiac fibroblasts proliferation with increased collagen synthesis and type I and type III collagen protein expressions as well as MMP-2 and MMP-9 activities and MMP-1 expression. AcSDKP inhibited cardiac fibroblasts proliferation induced by PDGF and reduced collagen synthesis and type I and type III collagen protein expression. AcSDKP also further up-regulated MMP-2 and MMP-9 activities and MMP-1 expression in cardiac fibroblasts induced by PDGF. CONCLUSION: AcSDKP inhibited proliferation and collagen synthesis and up-regulated matrix metalloproteinases activity or expression induced by PDGF, which was possibly related with the effect of AcSDKP anti-fibrosis.