细胞坏死关键调控蛋白RIP3在急性胰腺炎发病中的作用  

Role of RIP3 protein mainly regulating cell necrosis in pathogenesis of acute pancreatitis

作　　者：陆忠凯[1,2] 陈卫昌[1] 

机构地区：[1]苏州大学附属第一医院消化病科,江苏省215006 [2]南京医科大学附属苏州医院

出　　处：《江苏医药》2015年第5期523-524,I0001,共3页Jiangsu Medical Journal

摘　　要：目的探讨细胞坏死关键调控蛋白受体相互作用蛋白3(RIP3)在急性胰腺炎(AP)发病中的作用。方法 AP患者84例分为轻型AP(MAP组,52例)和急性坏死性胰腺炎(SAP组,32例),发病后1、3、5d取外周血5ml,提取单个核细胞,行半定量RT-PCR检测RIP3的表达。以20例健康体检者作为对照(C组)。结果 MAP组和SAP组发病后RIP3的表达均高于C组(P<0.05);发病后3d的RIP3的表达均达高峰(0.422±0.086和0.882±0.122),SAP组高于MAP组(P<0.05)。结论 RIP3参与AP的发病,可能与病情的严重程度相关。Objective To explore the role of receptor interaction protein 3（RIP3）mainly regulating cell necrosis in pathogenesis of acute pancreatitis（AP）.Methods The expressions of RIP3 in mononuclear cells of periphyral blood were detected by semi-quantitative RT-PCR in the patients with mild AP（group MAP,52 cases）and those with acute necrosis pancreatitis（group SAP,32 cases）on the 1st,3rd and 5th day after onset.Twenty healthy people were taken as the controls（group C）.Results The expression of RIP3 after onset was obviously higher in groups of MAP and SAP than that in group C（P〈0.05）and peaked on the 3rd day（0.422±0.086 and 0.882±0.122）,which was higher in group SAP than those in group MAP（P〈0.05）.Conclusion RIP3 participates in the pathogenesis of AP and may be associated with its severity.

关 键 词：受体相互作用蛋白3 急性胰腺炎 

分 类 号：R576[医药卫生—消化系统]