己酮可可碱对p38丝裂原激活蛋白激酶激活的影响  

EFFECTS OF PENTOXIFYLLINE ON ACTIVATION OF p38-MITOGEN-ACTIVATED PROTEIN KINASE

作　　者：汤展宏[1] 钱卫[2] 季晓芳[1] 林成新[3] 张驰[1] 江家树[1] 

机构地区：[1]广西医科大学第一附属医院ICU,南宁530021 [2]广西医科大学附属肿瘤医院麻醉科 [3]广西医科大学第一附属医院麻醉科

出　　处：《广西医科大学学报》2006年第6期895-897,共3页Journal of Guangxi Medical University

基　　金：广西科技厅自然科学基金资助项目(No.桂科自0135057)

摘　　要：目的:观察己酮可可碱(PTX)对p38丝裂原激活蛋白激酶(MAPK)激活的影响,探讨PTX保护内皮细胞单层通透性的机制。方法:建立内皮细胞单层损伤模型,随机分为脂多糖(LPS)-A组、LPS-B组、LPS+PTX-A组及LPS+PTX-B组,分别以不同终浓度LPS及PTX刺激不同时间,以Western印迹杂交技术检测内皮细胞p38MAPK活性。结果:LPS组,随着LPS刺激时间的延长及刺激浓度的增大,磷酸化的p38MAPK亮度逐渐增强;LPS+PTX组,磷酸化的p38MAPK亮度随着PTX刺激时间的延长及刺激浓度的增大而逐渐减弱。结论:PTX可通过降低p38MAPK的活性而起保护内皮细胞通透性的作用。Objective. To investigate the effects of pentoxifylline （PTX） on activation of p38 Mitogen-activated protein kinase, and to study the protective mechanism of PTX on endothel cell monolayer permeability. Methods. To observe the effect of PTX and LPS on the activity of p38Mitogen-activated protein kinase （p38MAPK） with different concentrations and times in HUVEC stimulated by LPS by western blot analysis in vitro cultured endothelial cell monolayer （ECM） in LPS-induced ECM injury model with human umbilical vein endothelial cells（HUVEC） in LPS-A group, LPS-B group, LPS＋ PTX-A group and LPS＋ PTX-B group. Result.The extent of p38MAPK phosphorylation in LPS group increased and that in LPS＋ PTX group decreased significantly with increasing concentrations and times. Conclusion. The protective effect of PTX on endothelial cell monolayer permeability may be associated with the inhibition of PTX to p38MAPK phosphorylation.

关 键 词：己酮可可碱 P38丝裂原激活蛋白激酶 脂多糖 

分 类 号：R363[医药卫生—病理学]