肝癌TAE后正常肝组织中PPAR-α和氧化应激指标的表达

摘要

Objective To investigate the roles of peroxisome proliferators-activated receptor-α (PPAR-α) and oxidative stress (OS) in hepatocyte injury after hepatic carcinoma transarterial catheter embolization (TAE). Methods Twenty-seven New Zealand white rabbit VX2 hepatocellular carcinoma (HCC) models were successfully established. They were randomly divided into three groups, Group Control, Group Contrast/Angiopgraphy and Group TAE. The rabbits in Group Angiography or TAE were injected with contrast agent or treated with TAE, respectively. The rabbits in the Group TAE and Group Angiography were sacrificed 10 hours after TAE treatment and contrast injection. The activity or content of oxidative stress indicators (SOD, CAT, GSH-Px and MDA) on paracancerous liver tissues were detected in all the groups by biochemical enzymatic assay. Immunohistochemical analysis was used to detect the expression of PPAR-α in liver tissues.Results Compared with the Group Control, no significant difference was revealed in the activity of antioxidant indexes SOD, CAT and GSH-Px in liver tissue or the content of MDA peroxidation product in Group Angiography (P＞0.05). Compared with the Group Angiography, the anti-oxidation indexes of SOD, CAT and GSH-Px in the liver tissue of the Group TAE group were significantly reduced; while the MDA content of the peroxidation product was significantly increased (P＜0.01). Compared with the Group Control, the expression of PPAR-hein Group Angiography showed decreasing trend, but the difference was not statistically significant (P＞0.05). Compared with the Group TAE, the expression of PPAR-atistica Group Angiography showed significant increased trend (P＜0.01). Conclusion In hepatocellular carcinoma after TAE, the expression of PPAR-α is reduced in paracancerous liver tissues. The activities of antioxidant indexes like SOD, CAT and GSH-Px are reduced, the content of MDA in peroxidation products is increased, and results in hepatocyte injury.%目的 探讨过氧化物酶体增殖物激活受体α(peroxisome proliferators-activated receptor-α,PPAR-α)和氧化应激(oxidative stress,OS)在肝癌经导管肝动脉栓塞术(TAE)后肝组织损伤中的作用机制.方法 成功建立新西兰大白兔VX2肝癌模型27只,编号法随机分为对照组、造影组、TAE组,每组9只.造影组和TAE组相同时间点注射造影剂后,TAE组进行TAE治疗10 h后处死实验兔,造影组于TAE组在相同时间(TAE手术时间+10 h)处死取材.在不同实验组癌旁肝组织中用生化酶学法检测肝组织中氧化应激指标[超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)和丙二醛(MDA)]的活力或含量;免疫组化法检测PPAR-α在不同组间肝组织中的表达情况.结果 造影组与对照组相比,肝组织抗氧化指标SOD、CAT和GSH-Px的活力有降低趋势,而过氧化产物MDA含量有升高趋势,两组比较差异无统计学意义(P＞0.05);造影组与TAE组比较,TAE组肝组织中抗氧化指标SOD、CAT和GSH-Px活力明显低于造影组,而过氧化产物MDA含量升高,差异有统计学意义(P＜0.01).与对照组相比,造影组PPAR-α的表达有降低趋势,但差异无统计学意义(P＞0.05);TAE组PPAR-α的表达量低于造影组,差异有统计学意义(P＜0.01).结论 肝癌TAE术后癌旁肝组织PPAR-α表达下降,抗氧化指标SOD、CAT和GSH-Px活力减低,过氧化产物MDA含量升高,可能是导致肝细胞受损、肝功能下降的作用机制之一.