JNK信号转导通路对白细胞介素-1β促肝星状细胞增殖的调控作用  

Regulatory effects of JNK transduction on interleukin-1β-induced proliferation in rat hepatic stellate cells

作　　者：张亚平[1] 姚希贤[1] 赵霞[1] 

机构地区：[1]河北医科大学第二医院消化内科,河北石家庄050000

出　　处：《中国病理生理杂志》2006年第6期1138-1141,共4页Chinese Journal of Pathophysiology

摘　　要：目的:探讨JNK信号转导通路在白细胞介素-1β(IL-1β)介导的促肝星状细胞(HSCs)增殖中的作用。方法:应用Western印迹法检测JNK的活化程度。应用活细胞计数试剂盒-CCK-8检测HSCs增殖并观察JNK特异性阻断剂SP600125对IL-1β促HSCs增殖的影响。结果:IL-1β有明显促大鼠HSCs增殖作用,而经JNK特异性阻断剂SP600125预处理后,IL-1β促HSCs增殖作用受到抑制(1·560±0·110vs1·427±0·113,P<0·05)。IL-1β以时间依赖方式激活JNK。IL-1β作用HSCs后0、5、15、30、60和120min,JNK活性分别为0·982±0·299、1·501±0·720、2·133±0·882、3·360±0·452、2·181±0·789、1·385±0·368。结论:IL-1β可刺激HSCs增殖,细胞内JNK信号转导通路参与了IL-1β促HSCs增殖作用。AIM： To study the action of JNK in stimulating proliferation in rat hepatic stellate cells （HSCs） induced by intedeukin -1β. METHODS： Activation of JNK was detected with Western blotting, while the proliferation of HSCs induced by interleukin-1β and the effect of JNK specific blockade SP600125 were measured with cell counting kit- 8. RESULTS： Intedeukin -1β up- regulated proliferation in rat HSCs, which was obviously inhibited by SP600125, compared with control group （without SP600125 treatment） （1.560±0.110）, the decrease was significant （1.427±0.113, P〈0.05）. Interleukin -1β activated JNK signaling pathway in a time- dependent manner. At the six time points （0, 5, 15, 30, 60 and 120 rain）, the JNK activities were 0. 982±0 . 299 , 1.501 ± 0.720, 2.133 ± 0.882, 3.360 ± 0.452, 2.181±0.789, 1.385 ± 0.368, respectively. CONCLUSION： Interleukin- 1β sthnulates proliferation in rat HSCs, and JNK signaling pathway is involved in this process.

关 键 词：信号转导 白细胞介素1 肝星状细胞 细胞增殖 

分 类 号：R363[医药卫生—病理学]