PPAR-α激动剂Wy14643减轻肝细胞系氧化应激损伤  

PPAR-α agonist Wy14643 alleviates oxidative damage in liver cells

作　　者：李金莲[1] 刘军锋 李娜[1] 栾海云[1] 

机构地区：[1]滨州医学院,山东烟台264003 [2]滨州市滨城区市立医院,山东滨州256600

出　　处：《基础医学与临床》2012年第11期1284-1287,共4页Basic and Clinical Medicine

基　　金：山东省自然科学基金(ZR2010HL068);烟台市科技发展计划项目(2011074)

摘　　要：目的探讨过氧化物酶体增殖物激活受体(PPAR)-α激动剂Wy14643对过氧化氢(H2O2)诱导HL7702肝细胞损伤的保护作用及其机制。方法 RT-PCR、Western blot分别检测H2O2损伤后HL7702肝细胞PPAR-αmRNA及蛋白表达。Wy14643预孵育细胞,观察其对H2O2损伤HL7702肝细胞活性、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性及NF-κB活化的影响。结果 H2O2可诱导HL7702细胞PPAR-αmRNA及蛋白表达降低,200和300μmol/L H2O2损伤后蛋白表达量由0.69±0.04分别降至0.48±0.05和0.38±0.03(P<0.01);Wy14643能够抑制H2O2诱导的HL7702细胞活性降低、SOD、CAT活性下降及NF-κB的激活。结论 Wy14643减轻H2O2诱导的肝细胞损伤,并增强细胞的抗氧化能力,可能与抑制NF-κB的活化有关。Objective To investigate the protective effects and mechanisms of peroxisome proliferators activated receptor（PPAR）-α agonist Wy14643 on HL7702 cells injured by H2O2.Methods The mRNA and protein expressions of PPAR-α in H2O2-damaged HL7702 cells were examined by RT-PCR and Western blot respectively.Pretreated with Wy14643 before H2O2 exposure,cell viabilities,superoxide dismutase（SOD） and catalase（CAT） activities,and NF-κB activation in HL7702 cells were detected.Results PPAR-α mRNA and protein expressions were decreased by H2O2 exposure.After 200 and 300 μmol/L H2O2 exposure,the protein expression level of PPAR-α reduced from 0.69±0.04 to 0.48±0.05 and 0.38±0.03 respectively（P0.01）.Pre-incubation by Wy14643,the decreased cell viabilities,SOD and CAT activities,and increased NF-κB activation in H2O2-damaged HL7702 cells were all inhibited.Conclusions The present study provides evidence that Wy14643 alleviates oxidative damage in HL7702 cells induced by H2O2 and enhances the cellular antioxidant capacity,which may be associated with the inhibition of NF-κB activation.

关 键 词：PPAR-Α WY14643 过氧化氢 HL7702细胞 氧化应激 

分 类 号：R363[医药卫生—病理学]