茯苓酸对SLT-Ⅱe诱导大鼠肠黏膜微血管内皮细胞分泌细胞因子的影响  

Effects of pachymic acid on the secretion of cytokines from rat intestinal microvascular endothelial cells induced by SLT-Ⅱe

作　　者：周宏超[1] 高立云[2] 范光丽[1] 刘钟杰[3] 穆祥[2] 

机构地区：[1]西北农林科技大学动物医学院,陕西杨凌712100 [2]北京农学院兽医学/中医药北京市重点实验室,北京昌平102206 [3]中国农业大学动物医学院,北京100094

出　　处：《中国兽医科学》2008年第10期884-888,共5页Chinese Veterinary Science

基　　金：国家自然科学基金项目(30671543);北京市自然科学基金项目(6021001);北京市属市管高等学校人才强教计划项目(BAHED)

摘　　要：将培养的大鼠肠黏膜微血管内皮细胞(RIMEC)分为正常对照组、SLT-Ⅱe对照组、不同浓度茯苓酸处理组,采用硝酸还原酶法和ELISA法测定了培养3、6、9和12 h时细胞培养上清液中NO、ET-1、PGI2、TXA2及PAF含量的变化,研究了中药复方有效成分茯苓酸对仔猪水肿病的治疗机制。结果显示,1、5、10μg/mL茯苓酸均可下调SLT-Ⅱe诱导的RIMEC NO、TXA2的分泌,10μg/mL茯苓酸可抑制SLT-Ⅱe诱导的RIMEC ET-1的分泌,使其分泌的ET-1含量接近正常水平;不同浓度茯苓酸对SLT-Ⅱe诱导RIMEC过量分泌PGI2、PAF无影响。表明,茯苓酸可通过抑制SLT-Ⅱe诱导肠黏膜微血管内皮细胞NO、ET-1及TXA2的过量分泌,缓解肠道微循环障碍,阻止血小板聚集,避免微血栓形成,从而达到治疗水肿病的目的。To elucidate the mechanism of pachymic acid treatment for swine edema disease,the cultured rat intestinal microvaseular endothelial cells（RIMEC） were divided into normal control group, SLT-Ⅱ e control group and various concentrations of treatment groups, and concentrations of NO, ET-1, PGI2, TXA2 and PAF from RIMEC induced by SLT-Ⅱ e for 3,6,9 and 12 h were measured by deoxidization enzyme and ELISA,respectively. The concentrations of 1,5 and 10μg/mL pachymic acid inhibited remarkably the secretion of NO and TXA2. Moreover 10μg/mL pachymic acid inhibited the secretion of ET-1. But pachymic acid had no inhibition for the secretion of pGI2 and PAF. Pachymic acid inhibited the secretion of NO,ET-1 and TXA2 and relieved intestinal microcirculation obstruction and microthrombus formation to cure swine edema disease.

关 键 词：茯苓酸 志贺样毒素Ⅱ型变异体 大鼠肠黏膜微血管内皮细胞 一氧化氮 内皮素一1 前列环素 血栓素A2 血小板活化因子 

分 类 号：S853.74[农业科学—临床兽医学] Q852.21[农业科学—兽医学]