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作 者:江海龙[1,2] 马丽群[1] 苏海明[1] 沈倩波[1] 葛冬云[1] 王海涛[1] 甘继宏[1]
机构地区:[1]兰州军区乌鲁木齐总医院心内科,830005 [2]空军总医院
出 处:《中华老年心脑血管病杂志》2012年第8期867-870,共4页Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
摘 要:目的探讨软脂酸(PA)诱导的血管内皮细胞凋亡中丝裂原活化蛋白激酶(MAPK)通路的作用。方法将人脐静脉内皮细胞(HUVEC)分对照组、PA组、MAPK通路干预组[分别先用p38抑制剂SB203580、氨基末端激酶(JNK)抑制剂PD98059、细胞外信号调节激酶(ERK)抑制剂SP600125干预]再分为PA+SB组、PA+PD组、PA+SP组。流式细胞仪检测细胞凋亡率;Western blot法检测caspase-3、磷酸化p38、JNK和ERK1/2表达水平;分光光度法检测caspase-3的活性。结果与对照组比较,PA组、PA+SB组、PA+PD组、PA+SP组HUVEC凋亡及caspase-3表达和活性明显增加,PA组磷酸化p38MAPK表达明显增加(P<0.05)。与PA组比较,PA+SB组HUVEC细胞凋亡率、caspase-3表达和活性明显降低(P<0.05);而PA+PD组和PA+SP组HUVEC凋亡率、caspase-3表达和活性无明显变化(P>0.05)。结论 PA通过p38MAPK通路促进内皮细胞凋亡。Objective To study the role of mitogen-activated protein kinase(MAPK) pathway in palmitic acid(PA)-induced apoptosis of vascular endothelial cells. Methods Cultured HUVEC were divided into control group, PA group, and MAPK pathway interference group. Two hours af- ter interfered with M199 culture fluid containing p38 inhibitor SB203580, amino terminal kinase (JNK) inhibitor PD98059,and extracellular signal regulating kinase(ERK) inhibitor SP600125. The MAPK pathway interference group was further divided into PA+SB group,PA+PD group, PA+SP group and incubated for 46 h by adding 400 vmol/L PA. Apoptotic rate of HUVEC was assayed by flow cytometry. Expressions of apoptotic protein caspase-3 and phosphorylated p38, JNK,ERK1/2 were detected by Western blot. Caspase-3 activity was measured by spectropho- tography. Results The apoptotic rate of HUVEC and the caspase-3 expression and activity levels were significantly higher in PA, PA+ SB, PA+PD and PA+SP groups than in control group(P〈0.05). The expression level of phosphorylated p38 was significantly higher while the apoptotic rate of HUVEC and the caspase-3 expression and activity levels were significantly lower in PA group than in PA+ SB, PA + PD and PA + SP groups (P 〈0.05). No significant difference was found in apoptotic rate of HUVEC and caspase-3 expression and activity levels, and in JNK and ERK1/2 protein expression levels between PA+PD and PA+SP groups(P〉0.05). Conclusion PA promotes apoptosis of vascular endothelial cells via the p38 MAPK pathway.
关 键 词:棕榈酸 丝裂原激活蛋白激酶类 P38丝裂原活化蛋白激酶类 内皮 血管 细胞凋亡 转录因子
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