摘要
为探索肠黏膜微血管内皮细胞在仔猪水肿病发生机制中的作用,将培养的肠黏膜微血管内皮细胞分为对照组、不同浓度SLT-Ⅱe处理组等5个组,采用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、P-选凝素、sICAM-1及TNF-α浓度的变化。结果表明,1、10μg/mL SLT-Ⅱe诱导内皮细胞作用12 h时NO的分泌浓度是对照组NO分泌浓度的3倍。1μg/mL SLT-Ⅱe作用12 h时ET-1、P-选凝素、sICAM-1及TNF-α的浓度分别是相应对照组的4.6、2.8、2.8、1.8倍。由此可见,SLT-Ⅱe通过诱导肠黏膜微血管内皮细胞NO、ET-1、P-选凝素、sICAM-1及TNF-α的过量分泌,NO/ET-1比值下降,引起肠道微循环障碍,炎症反应,导致水肿病的发生。SLT-Ⅱe诱导大鼠肠黏膜微血管内皮细胞损伤的最佳模型剂量为1μg/mL。
To explore the mechanism of swine edema,the cultured rat intestinal microvascular endothelial cells（RIMECs） were divided into control group and different concentration of SLT-Ⅱe groups.Secretions of NO,ET-1,P-selectin,sICAM-1 and TNF-α by RIMECs were determined by ELISA at 3,6,9,and 12 h post-induction.The results showed that 1 and 10 μg/mL SLT-Ⅱe increased the NO production in RIMECs by 3 times for 12 h incubation.1 μg/mL SLT-Ⅱe could increase the secretion of NO in RIMECs by 3 times,ET-1,P-selectin,sICAM-1and TNF-α by 4.6,2.8,2.8 amd 1.8 times for 12 h,compared with control group,respectively.The results revealed that SLT-Ⅱe caused swine edema by over inducing the secretion of NO,ET-1,P-selectin,sICAM-1and TNF-α in RIMECs,and dramatically decreasing the NO/ET-1 ratio,which might result in intestinal microcirculation obstruction.The best model concentration of SLT-Ⅱe to damage the RIMECs was found to be 1 μg/mL.
出处
《中国兽医科学》
CAS
CSCD
北大核心
2009年第8期738-742,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)
