摘要
目的:探讨促吞噬肽及其拮抗剂诱导炎性介质肿瘤坏死因子(tumor necrosis factor,TNF)、白介素-1(interleukin-1,IL-1)释放在急性胰腺炎(acute pancreatitis,AP)病情发展中的作用.方法:SD大鼠5组每组24只,分别为对照组、促吞噬肽组、A P组、A P+促吞噬肽组、AP+促吞噬肽拮抗剂组.4%牛磺胆酸钠经胆胰管内注射建立AP模型,促吞噬肽及其拮抗剂组(75μg/kg)于模型建立后20 min后从股静脉注入.按随机原则在制模后3、6、12 h处死,甲醛固定胰腺组织行HE染色观察胰腺病理变化;分离血清ELISA法测定IL-1和TNF浓度.结果:AP各组TNF、IL-1浓度均比对照组明显升高;AP+促吞噬肽组各时间段TNF、IL-1浓度均较单纯AP组升高;AP+促吞噬肽拮抗剂组在制模后6、12 h TNF、IL-1浓度明显降低,在制模后3 h无明显影响;AP模型病理学评分与TNF浓度、IL-1浓度存在正相关关系.结论:在大鼠AP模型中促吞噬肽使TNF、IL-1浓度升高,胰腺炎症反应加重;应用促吞噬肽拮抗剂可减少TNF、IL-1释放,使胰腺炎症反应减轻.
AIM： To investigate the role of tuftsin and its inhibitor in acute pancreatitis（AP）. METHODS： Twenty-four SD rats were randomly divided into five groups： a blank control group, a tuftsin group, an AP group, an AP ＋ tuftsin group, and an AP ＋ tuftsin inhibitor group. AP was induced in rats by injecting sodium taurocholate in the pancreatic duct. Tuftsin or its inhibitor（75 μg/kg） was injected via the femoral vein at 20 min after model induction. At 3, 6, and 12 h after model induction, pancreatic samples were taken for HE staining to detect pancreatic pathology, and serum samples were taken for tumor necrosis factor（TNF） and interleukin-1（IL-1） measurement by ELISA. RESULTS： Serum levels of TNF and IL-1 were significantly higher in the AP group than in the control group, and in the AP ＋ tuftsin group than in the AP group. Serum levels of TNF and IL-1 were significantly decreased in the AP ＋ tuftsin inhibitor group at 6 h and 12 h, but showed no significant change at 3 h. Correlation analysis showed that serum levels of TNF/IL-1 were positively correlated with pancreatic pathology. CONCLUSION： Tuftsin accelerates the development of AP by inducing TNF and IL-1. The inhibitor of tuftsin can alleviate AP by downregulating TNF and IL-1.
出处
《世界华人消化杂志》
CAS
2016年第22期3404-3409,共6页
World Chinese Journal of Digestology
