摘要
目的探讨过氧化物酶体增殖物激活受体γ(PPARγ)激动剂吡格列酮在大鼠胰腺缺血再灌注损伤中的作用及机制。方法建立大鼠胰腺缺血再灌注损伤模型,将40只SD大鼠随机分为假手术组(S组)、缺血再灌注损伤组(IR组)、吡格列酮预处理组(PGZ组)及吡格列酮+GW9662预处理组(PGZ+GW9662组),每组10只。再灌注后,取静脉血检测血淀粉酶、脂肪酶水平,取胰腺组织检测核因子-κB(NF-κB)、Bcl-2蛋白、超氧化物歧化酶(SOD)表达。结果与S组相比,其余3组血淀粉酶和脂肪酶水平、胰腺组织NF-κB活性均明显升高,SOD、Bcl-2表达则明显降低(F=21.72-356.76,q=4.37-10.13,P〈0.05);与IR组相比,PGZ组血淀粉酶、脂肪酶水平和胰腺组织NF-κB活性均明显降低,SOD、Bcl-2表达明显升高(q=3.45-8.72,P〈0.05);而PGZ+GW9662组与IR组相比差异无统计学意义(q=0.16-1.13,P〉0.05);与PGZ组相比,PGZ+GW9662组血淀粉酶、脂肪酶水平和胰腺组织NF-κB活性表达明显增加,SOD、Bcl-2表达明显降低(q=3.77-8.98,P〈0.05)。结论PPARγ激动剂吡格列酮可能是通过PPARγ途径上调SOD的活性、Bcl-2表达及下调NF-κB表达,对胰腺缺血再灌注损伤起保护作用。
Objective To investigate the effect of pioglitazone-a peroxisome proliferator-activated receptor γ (PPARγ) activator on pancreatic ischemia reperfusion injury and its mechanism in the rat. Methods A model of ischemia reperfusion injury (IRI) in pancreas was established in 40 SD rats, which were evenly randomized to four groups as sham-operation group (group A), ischemia reperfusion group (group B), pioglitazone group (group C) and pioglitazone+GW9662 group (group D). Serum diastase and lipase levels were determined, the pancreas tissue was removed for NF κB, Bcl 2 and SOD detections. Results Compared with group A, the serum levels of diastase, lipase and the activities of NF-κB in the other three groups were significantly increased, and the expressions of Bc12andSODdeereased(F=21.72 356.76,q=4.37 10.13,P〈0.05); Compared with groupB, the diastase, lipase and the activities of NF-κB in group C were significantly decreased, and Bcl 2 and SOD increased (q=3. 45-8. 72 ,P %0.05) ; Compared with group C, the diastase, lipase, and the activities of NF κB in group D were significantly increased, and Bcl-2 and SOD in group D decreased (q=3.77-8.98,P〈0.05). Conclusion PPARγactivator-pioglitazone-protects against IRI in pancreas is probably through up-regulating Bel-2 and SOD and down-regulating NF-κB activation.
出处
《青岛大学医学院学报》
CAS
2009年第5期427-429,共3页
Acta Academiae Medicinae Qingdao Universitatis