Effect of protein kinase C(PKC) inhibitor on the proliferation of human embryonic pulmonary fibroblasts induced by chrysoffie

Abstract

Objective To explore the role of protein kinase C(PKC) signal pathway in the proliferation of human embryonic pulmonary fibroblasts (HEPF) caused by chrysotile-induced alveolar macrophage ( AM )-derived factors. Method s MTT color response method to measure the proliferation of HEPF stimulatod by the snpernatants of chrysotile-treated rabbit AMs in vitro was used and the effect of PKC inhibitor on it was observed. Blank control,normal control( AM ), negative ( TiO2 ) and positive control ( SiO2 ) were set up Results The supernatants of chrysetile-treated rabbit AMs significantly stimulated the proliferation of HEPF. The quantity of the proliferation increased with dose-effect relationship( r = 0. 671 8, P SiO2 >TiO2( P < 0.01 ) ,their differences were significant( P < 0.01 ). The proliferation of chrysotile-indnced HEPF was inhibited by PKC inhibitor(C25H24N4O2) with significant dose-effect relationship( P < 0.01 ), and the inhibiting intensity of HEPF in chrysetile group was higher than that in the different control group. Conclusion The supernatants of chrysotile-treated AMs could significantly stimulate the proliferation of HEPF with dose-effect relationship ,while PKC inhibitor could inhibit this effect( P < 0.01 ). There may be some bioactive factors in the supernatant to stimulate the proliferation of HEPF through PKC signal pathway. Key words: Pcotein kinase C; Chrysotile; Alveolar macrophage; Human embryonic pulmonary fibrob lasts; Cell proliferation