Erk信号传导通路调控乙醛刺激的肝星状细胞Ⅰ型胶原分泌的研究

Effect of extracellular-regulated kinase signaling pathways on type Ⅰ collagen synthesis stimulated by acetaldehyde in rat hepatic stellate cells

目的 探讨Erk信号传导通路调控乙醛刺激的肝星状细胞Ⅰ型胶原分泌的影响。方法 用链霉蛋白酶和胶原酶原位灌流 ,Metrizamide密度梯度离心分离大鼠肝星状细胞 ,采用PD980 5 9阻断乙醛激活的肝星状细胞Erk活性 ,以ELISA法定量测定细胞上清Ⅰ型胶原。结果 PD980 5 9在 2 0 μmol/L时可影响HSCⅠ型胶原分泌 ,但无统计学意义 (P >0 0 5 ) ,5 0、10 0 μmol/L抑制作用明显 (P <0 0 5或P <0 0 1) ,呈剂量 效应关系。 结论 PD980 5 9对乙醛刺激的HSCⅠ型胶原分泌具有抑制作用 ,提示Erk信号传导通路是调控乙醛刺激的HSCⅠ型胶原分泌重要通道。

Objective To study the effect of extracellular regulated kinase signaling pathways on type Ⅰ collagen synthesis stimulated by acetaldehyde in rat hepatic stellate cells(HSC) Methods HSCs were isolated and cultured from liver of Sprague Dawdey rats by in situ perfusion with pronase and collagenase,and density gradient centrifugation with metrizamide Type Ⅰ collagen was detected by ELTSA while HSC was stimulated by acetaldehyde pre disposed in different doess of PD98059 Results PD98059 with a concentration of 20 μmol/L suppressed type Ⅰ collagen synthesis of HSC stimulated by acetaldehyde( P >0 05),and the inhibition of PD98059 with the concentration of 50μmol/L and 100μmol/L was significant( P <0 05 or P <0 01),which turned out to be a dose dependant effect Conclusion PD98059 had an inhibitory effect on type Ⅰ collagen synthesis of HSC stimulated by acetaldehyde,which demonstrated the importance of Erk on the aspect of HSC's signal trans mission