摘要
探讨油酰乙醇胺(OEA)对氧化性低密度脂蛋白(ox-LDL)诱导的人脐静脉内皮细胞(HUVEC)坏死的影响及对ox-LDL诱导的小鼠巨噬细胞(RAW264.7)内炎性因子表达变化的影响.实验用ox-LDL诱导HUVEC坏死和RAW264.7细胞内炎性反应;显微镜下观察细胞形态,并收集细胞进行Annexin V/PI-FITC染色,流式细胞分析细胞坏死率;采用实时定量PCR(real-ti me PCR)和酶联免疫吸附剂检测(ELISA)测定mRNA和蛋白水平表达的变化.结果显示:OEA能缓解ox-LDL诱导的HUVEC的坏死,并能呈浓度依赖性的上调HUVEC内过氧化物酶体增殖激活受体α(PPAR-α)和SIRT-1的表达;OEA降低ox-LDL诱导的RAW264.7肿瘤坏死因子α(TNF-α)和CRP mRNA表达的升高,及降低ox-LDL诱导的促动脉粥样硬化因子M-CSF mRNA表达的升高,同时升高ox-LDL诱导SIRT-1表达的降低.实验结果表明,OEA通过激活PPAR-α和抗炎通路对动脉粥样硬化有一定的作用.
The effect of OEA on ox-LDL induced atherosclerosis response was investigated.HUVEC and RAW 264.7 cells treated with ox-LDL were used to induce necrosis and inflammation,respectively.Cell necrosis was detected by AnnexinⅤ/PI-FTIC staining and flow cytometer.The expression level of mRNA and protein were detected by quantitative real-time PCR and ELISA.Data showed that,in HUVEC cells,OEA inhibits necrosis induced by ox-LDL through activation of PPAR-α and SIRT-1 expression.In RAW 264.7 cells,OEA decreased the expression levels of inflammatory cytokines,including TNF-α and CRP,and pro-atherosclerosis factor,M-CSF.Furthermore,OEA treatment reversed the expression of SIRT-1,which was suppressed by ox-LDL.The data suggests that OEA played a certain role on atherosclerosis through activation of PPAR-α and anti-inflammatory pathway.
出处
《厦门大学学报（自然科学版）》
CAS
CSCD
北大核心
2011年第1期127-131,共5页
Journal of Xiamen University：Natural Science
