摘要
目的:探讨PPAR-α在肝癌经肝动脉栓塞术(TAE)后肝功能异常中的作用机制。方法:建立新西兰大白兔VX2肝癌动物模型26只,模型成功率为86%(24/28),将兔VX2肝癌动物模型随机分为栓塞组12只,造影组12只,TAE术后8 h各组兔同时处死,取肿瘤旁取正常肝组织,制作石蜡切片,进行HE染色以及免疫组化,检测PPAR-α在肝组织中的表达。结果:栓塞组阳性细胞数介于51%-85%,阳性评估为++/+++,造影组阳性细胞数介于10%-30%,阳性评估为+/++。统计学分析表明TAE术后,癌旁肝组织中PPAR-α的表达明显高于造影组(P<0.05)。结论:TAE后,PPAR-a在肿瘤周围肝细胞中的表达明显增加,可能机制为癌旁正常肝组织缺血缺氧,从而导致PPAR-α高表达。
Objective: To investigate the function mechanism of PPAR -α in liver cancer on abnormal liver function after transcatheter arterial embolization(TAE). Methods: VX2 hepatic cancer model in 26 New Zealand white rabbits model were established with 86% successful rate(24/28). VX2 hepatic cancer models in rabbits were randomly divided to embolization group(12), angiography group(12). Rabbits of very group were sacrificed 8 hours after TAE. Liver tissues surrounded HCC were collected to make paraffin section, and the expression of PPAR-α in hepatic tissue was detected after hematoxylin & eosin(HE)staining and immunohistochemistry. Results: Positive cells in embolization group ranged from 51%-85% with a positive assessment ++ / +++;positive cells in angiography group were between 10%-30% with a positive assessment of + / ++. Statistical analysis showed that the PPAR-α expression in cancer adjacent hepatic tissue of embolization group was significantly higher than angiography group(P〈0.05). Conclusion: After TAE, PPAR-α expression in tumor adjacent hepatic tissue increased significantly. The possible reason of high expression of PPAR-α might be hypoxia ischemia of cancer adjacent normal tissues.
出处
《大理大学学报》
CAS
2016年第10期67-70,共4页
Journal of Dali University
基金
国家自然科学基金资助项目(81241131)
云南省教育厅科学研究基金资助项目(2013J113)
关键词
PPAR-Α
肝癌
动脉栓塞术
肝功能
PPAR -α
liver cancer
arterial embolization
liver function