过氧化物酶体增殖物激活受体-γ激动剂对急性胰腺炎大鼠肺损伤的保护机制研究  

Protection of PPAR-γ agonists on lung injury in rats with acute pancreatitis

作　　者：陆贝[1] 于源泉[2] 殷俊杰[1] 蔡阳[1] 

机构地区：[1]杭州市第一人民医院肝胆外科,浙江杭州310006 [2]浙江大学医学院附属第二医院肝胆外科,浙江杭州310009

出　　处：《中国现代医生》2017年第18期38-41,F0003,共5页China Modern Doctor

基　　金：浙江省医药卫生科技计划项目(2014KYA172)

摘　　要：目的探讨过氧化物酶体增殖物激活受体-γ激动剂对胰腺炎大鼠肺损伤的保护作用及调节机制。方法 72只大鼠随机分为假手术组、模型组和罗格列酮组,各组再分为术后6 h、12 h、24 h组。模型组采用两次腹腔注射L-精氨酸制备SAP模型,罗格列酮组术后30 min静脉注射10%罗格列酮6 mg/kg,假手术组腹腔注射等体积生理盐水。观察大鼠肺病理改变,测定肺TLR4、NF-κB、肺髓过氧化物酶活性、肺干/湿重比、血清TNF-α、IL-1β、IL-6含量。使用重复测量方差分析,SNK-q检验比较差异。结果 ROSI组大鼠肺组织病理损害较SAP组减轻;与SAP组比较,肺内NF-κB、TLR4蛋白下降(P<0.05),髓过氧化物酶活性及肺干/湿重比降低(P<0.05);ROSI组外周血IL-1β、IL-6、TNF-α含量与SAP组比较明显下降(P<0.05)。结论 PPAR-γ激动剂能减轻急性胰腺炎大鼠肺组织的损伤,抑制NF-κB、TLR4表达,降低促炎细胞因子水平,推测PPAR-γ激动剂对NF-κB/TLR4通路的调节可能是胰腺炎的保护机制之一。Objective To find the protection of PPAR-γ agonists on injured lung cells in rats and mechanism during acute pancreatitis. Methods Rats were divided randomly into three groups： sham operation group, SAP model group, rosiglitazone group. Each group was divided into 6 h, 12 h, and 24 h group after operation. SAP rats model were made via twice peritoneal injection of L-arginine. Rats in ROSI group were injected with 6 mg/kg of 10% rosiglitazone via femoral vein 30 min after operation. Sham operation group rats were peritoneally injected of same volume NS as SAP group. Pathological changes of lung tissue, TLR4, NF-κB, MPO, dry and wet ratio in lung tissue were tested. Serum TNF-α, interieukin-1β, interieukin-6 were also determined. Results The pathological injuries of lung cell were re- lieved in ROSI group compared with SAP group. There were statistic differences in TLR4, NF-κB, MPO, dry and wet ratio in lung between ROS1 and SAP group, which were decreased in ROSI group compared with SAP group（P〈0.05）. TNF-α, IL-1β, IL-6 were decreased in ROSI group compared with those in SAP group（P〈0.05）. Conclusion The lung tissue injury during SAP may relived by PPAR-γ agonists, and also decrease NF-kappa B, TLR4 and inflammatory cy- tokines. The probable reason is that PPAR-γagonists protect pancreas by adjusting NF-κB/TLR4 signal pathway.

关 键 词：急性胰腺炎 过氧化物酶体增殖物激活受体 核转录因子-ΚB TOLL样受体 

分 类 号：R576[医药卫生—消化系统]