摘要
目的: 观察用特异性c Jun氨基末端激酶(c JunN terminalkinase,JNK)特异性阻断剂SP600125阻断JNK信号传导通路对乙醛刺激的大鼠肝星状细胞(Hepaticstellatecell,HSC)凋亡的影响.方法: 体外培养大鼠HSC株;用不同浓度的SP600125(20, 60, 100μg/L)对乙醛( 200μmol/L)刺激的大鼠HSC进行处理,分别以DNA片段凝胶电泳及流式细胞仪检测细胞凋亡,用WesternBlotting法检测JNK激酶的活性变化.结果: 不同浓度的SP600125 (终浓度为20, 60, 100μg/L)对乙醛刺激的HSC内p JNK的水平有明显下调作用,强度呈剂量依赖关系,同乙醛组相比有显著性差异[MVI: ( 35. 6±0 .9), (24. 4±1 .1), (3. 4±0. 2)vs(48. 2±0 .9),P<0 05];同时SP600125具有促进HSC凋亡的作用: 空白对照组及乙醛组中细胞凋亡率为[ (2. 0±0 .2)%和(6. 0±0. 5 )% ,两者有显著性差异(P<0 .05 ) ],经SP600125处理后细胞凋亡率上升[分别为( 11 .1±0. 4 )%, ( 26. 9±0 .9 )%, ( 33. 1±1 3)%,P<0. 05],同乙醛组相比有显著性差异(P<0. 05 ).结论: SP600125通过阻断JNK通路促进HSC凋亡,故JNK信号通路可能参与了HSC的凋亡.
AIM: To study the effects of SP600125,a specific blocking agent of c-Jun N-terminal kinase (JNK),on the apoptosis in rat hepatic stellate cells (HSC).METHODS: Rat hepatic stellate cells stimulated by acetaldehyde were incubated with different concentrations of SP600125 in vitro.The changes of apoptosis were analyzed by agarose gel eletrophoresis of DNA fragmentation and flow cytometry and the activity of JNK was measured by Western blot. RESULTS: SP600125 at different concentrations (20 ng/mL,60 ng/mL and 100 ng/mL) not only suppressed the activity of JNK [MVI: (35.6±0.9),(24.4±1.1),(3.4±0.2) vs (48.2±0.9),P<0.05],but also increased apoptosis of HSC [(11.1±0.4)%,(26.9±0.9)%,(33.1±1.3)% vs (6.0±0.5)%,P<0.05].CONCLUSION: The inhibitory effect of SP600125 on JNK binding activity may be involved in the apoptosis of HSC.
出处
《第四军医大学学报》
北大核心
2005年第10期915-918,共4页
Journal of the Fourth Military Medical University
基金
全军"十五"医药卫生科研基金(01MB037)
