摘要
目的探究秋水仙碱调控炎症因子在急性出血坏死性胰腺炎大鼠模型保护机制。方法选取50只雄性斯普拉格-道利大鼠,采用随机数字表法分为正常对照组、未治疗组、30 mg/kg组、50 mg/kg组和100 mg/kg组,每组10只。除正常对照组外各组大鼠使用牛磺胆酸钠制成急性出血坏死性胰腺炎大鼠模型,术前1 h通过舌下静脉给三个治疗组大鼠使用对应剂量的秋水仙碱治疗。采用HE染色观察组胰腺组织病理改变;采用酶联免疫吸附试验(ELISA)检测大鼠外周血中白细胞介素-6(IL-6)、白细胞介素-10(IL-10)、降钙素基因相关肽(CGRP)水平和肿瘤坏死因子-α(TNF-α)水平;采用蛋白质印迹检测各组大鼠胰腺组织中IL-6、IL-10、降钙素基因相关肽(CGRP)水平和TNF-α表达情况。结果HE染色观察发现正常对照组胰腺结构完整,未出现炎症浸润,未治疗组出现严重水肿、炎性浸润,细胞出现明显坏死,同时还伴随脂质空泡,使用秋水仙碱治疗各组炎性浸润、坏死细胞明显减少,基本无脂质空泡。相比正常对照组,未治疗组大鼠外周血及胰腺组织中IL-6、CGRP和TNF-α水平均显著升高(P<0.05),外周血及胰腺组织中IL-10水平显著降低(P<0.05)。相比未治疗组,使用秋水仙碱处理各组IL-6、CGRP和TNF-α水平均显著降低(P<0.05),且100 mg/kg组<50 mg/kg组<30 mg/kg组(P<0.05);相比未治疗组,使用秋水仙碱处理各组外周血及胰腺组织中IL-10水平显著升高(P<0.05),且100 mg/kg组>50 mg/kg组>30 mg/kg组(P<0.05)。结论秋水仙碱可以治疗急性出血坏死性胰腺炎,其作用机制可能与抑制大鼠体内炎症反应及改善胰腺血循环相关,且在一定剂量范围内呈剂量依赖性。
Objective To explore the protective mechanism of colchicine(COLC)for rat models of acute hemorrhagic necrotizing pancreatitis(AHNP)by regulating inflammatory factors.Methods Fifty male Sprague-Dawley rats were enrolled and divided into normal control group,untreated group,30 mg/kg group,50 mg/kg group and 100 mg/kg group by random number table method,10 cases in each group.Except for normal control group,AHNP rat models were made into by sodium taurocholate in the other groups.At 1 h before surgery,rats in the three treatment groups were treated with the corresponding dose of COLC through the sublingual vein.The pathological changes of pancreas tissues were observed by HE staining.The levels of interleukin-6(IL-6),interleukin-10(IL-10),calcitonin gene-related peptide(CGRP)and tumor necrosis factor-α(TNF-α)in peripheral blood were detected by enzyme-linked immunosorbent assay(ELISA).The expression levels of IL-6,IL-10,CGRP and TNF-αin pancreas tissues of each group was detected by Western blot.Results It was found by HE staining that pancreas structures were intact in normal control group,and there was no inflammatory infiltration.In untreated group,there was severe edema and inflammatory infiltration.There was significant cells necrosis,accompanied with lipid vacuoles.The inflammatory infiltration and necrotic cells were significantly decreased in each group treated with COLC,and there were basically no lipid vacuoles.Compared with normal control group,levels of IL-6,CGRP and TNF-αin peripheral blood and pancreas tissues were significantly increased(P<0.05),while IL-10 level in peripheral blood and pancreas tissue was significantly decreased in untreated group(P<0.05).Compared with untreated group,levels of IL-6,CGRP and TNF-αwere significantly decreased in each group treated with COLC(P<0.05),which were the lowest in 100 mg/kg group,followed by 50 mg/kg group and 30 mg/kg group(P<0.05).Compared with untreated group,IL-10 level in peripheral blood and pancreatic tissues was significantly increased in each gr
作者
张楠
梁盟
崔娜
陈治
于占彪
ZHANG Nan;LIANG Meng;CUI Na;CHEN Zhi;YU Zhan-biao(Department of Critical Care Medicine,Affiliated Hospital of Hebei University,Baoding,Hebei,071000,China;Hepatobiliary Surgery,Affiliated Hospital of Hebei University,Baoding,Hebei,071000,China)
出处
《现代消化及介入诊疗》
2020年第8期1060-1063,1067,共5页
Modern Interventional Diagnosis and Treatment in Gastroenterology
基金
保定市科技计划自筹经费项目(1941ZF085)。
关键词
胰腺炎
秋水仙碱
炎症因子
急性出血坏死
Pancreatitis
Colchicine
Inflammatory factor
Acute hemorrhagic necrosis
