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目的:探讨生长抑素对大鼠重症急性胰腺炎(SAP)时炎性调控作用及其机制。方法:逆行胰胆管注射牛磺胆酸钠(TAC)制备SAP模型。动物分为假手术组(SO组),生理盐水处理组(SAP组)和奥曲肽治疗组。各组动物术后3、6、12 h剖杀,检测肝组织中Toll-样受体(TLR)24 mRNA和细胞核转录因子(NF-κB)的表达情况。结果:与SO组比较,胰腺炎组大鼠TLR2,4 mRNA于3 h开始升高,于12 h达高峰(P均<0.01);肝组织中NF-κB于3 h开始表达增强,6 h达高峰。治疗组肝组织中的TLR2,4 mRNA及NF-κB各时点表达均降低(P<0.05)。结论:生长抑素对SAP时炎症反应有调控作用。其机制可能与抑制Toll受体和NF-κB表达,降低瀑链式炎症反应有关。
Objective: To investigate the effect and mechanism of somatostatin on inflammation in rats with severe acute pancreatitis (SAP). Methods: SAP model was established by injecting sodium taurocholate (TAC) into pancreaticobiliary duct. Animals were divided into sham group (SO group), saline group (SAP group) and octreotide treatment group. The animals were sacrificed at 3, 6, 12 h after operation to detect the expression of Toll-like receptor (TLR) 24 mRNA and nuclear transcription factor (NF-κB) in liver tissue. Results: Compared with SO group, TLR2,4 mRNA in pancreatitis group began to rise at 3 h and reached the peak at 12 h (P <0.01). The expression of NF-κB in liver tissue increased at 3 h, Peak. The expressions of TLR2, 4 mRNA and NF-κB in the liver of the treated group were all decreased (P <0.05). Conclusion: Somatostatin has a regulatory effect on inflammatory response in SAP. The mechanism may be related to the inhibition of Toll-like receptor and NF-κB expression and the decrease of cascade inflammation.