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目的 探讨内毒素在肝脏缺血再灌注损伤中的作用。方法 Wister大鼠随机分为 :内毒素组 ,肝脏缺血再灌注组 (HIR组 ) ,肝脏缺血再灌注复合内毒素血症组 (HIRE组 )。内毒素组自阴茎背静脉注射大肠杆菌内毒素 (LPS) 1 0mg/kg ;HIR组将肝左叶及肝中叶入肝血流阻断 60min后再灌注 ;HIRE组将肝左叶及肝中叶入肝血流阻断 60min后再灌注 ,同时自阴茎背静脉注射LPS1 0mg/kg。分别采用EMSA、免疫组化法及赖氏法检测再灌注后 1,3 ,12h肝脏组织中NF -κB结合活性、TNF -α的蛋白表达及血浆中ALT含量。结果 内毒素组NF -κB无明显激活 ,TNF -α无表达 ,血浆中ALT含量轻度升高 ;HIR组NF -κB活性仅于伤后 1、3h轻度增加 ,TNF -α有表达 ,ALT水平升高 ;与内毒素组及HIR组相比较 ,HIRE组损伤后NF -κB结合活性明显升高 ,至少可维持 12h ,同时肝组织TNF -α表达明显增加 ,血浆中ALT含量亦明显升高。结论 内毒素在HIR中可加重肝脏损伤 ,其机制可能是通过对NF -κB的双重激活引起肝内TNF -α等炎症相关细胞因子表达增加 ,从而加重肝脏损伤。
Objective To investigate the role of endotoxin in hepatic ischemia-reperfusion injury. Methods Wister rats were randomly divided into four groups: endotoxin group, hepatic ischemia / reperfusion group (HIR group) and hepatic ischemia / reperfusion combined endotoxemia group (HIRE group). The endotoxin group was injected with E.coli endotoxin (LPS) 10 mg / kg from the dorsal penile of the penis. The HIR group was reperfused 60 minutes after the occlusion of the hepatic lobe and middle hepatic artery, and the HIRE group Hepatic blood flow was blocked 60 minutes after reperfusion, at the same time from the dorsal penile vein injection of LPS1 0mg / kg. EMSA, immunohistochemistry and Lai’s method were used to detect NF-κB binding activity, TNF-α protein expression and plasma ALT content in liver tissue at 1, 3, and 12 h after reperfusion. Results No significant activation of NF-κB was found in endotoxin group, but TNF-α was not expressed and ALT level in plasma was slightly increased. The activity of NF-κB in HIR group was only slightly increased at 1h and 3h after injury, while TNF- Compared with the endotoxin group and the HIR group, the NF-κB binding activity of HIRE group was significantly increased, at least for 12h, while the expression of TNF-α in liver tissue was significantly increased and ALT level in plasma was also significantly increased . Conclusions Endotoxin can aggravate liver injury in HIR. The possible mechanism is that hepatic injury may be exacerbated by the increased expression of inflammatory cytokines, such as intrahepatic TNF-α, caused by double activation of NF-κB.