大黄素对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 emodin on the secretion of NO,ET-1,PGI2,TXA2,P-selectin and sICAM-1 in rat intestinal microvascular endothelial cells induced by SLT-Ⅱe

为探索中药复方主要成分大黄素对仔猪水肿病的疗效机制,将培养的肠黏膜微血管内皮细胞分为对照组、SLT-Ⅱe组、不同浓度大黄素处理组等5个组,采用ELISA法分别测定了培养3、6、9和12h时细胞培养上清液中NO、ET-1、PGI2、TXA2、P-选凝素及sICAM-1浓度的变化。结果显示,10μg/mL大黄素可下调SLT-Ⅱe诱导的大鼠肠黏膜微血管内皮细胞NO、ET-1及P-选凝素的分泌,12h内使NO、ET-1及P-选凝素的分泌浓度接近正常水平;1、5、10μg/mL大黄素不能下调SLT-Ⅱe诱导的大鼠肠黏膜微血管内皮细胞PGI2、TXA2及sICAM-1的分泌。结果表明,大黄素通过抑制SLT-Ⅱe诱导肠黏膜微血管内皮细胞NO、ET-1、P-选凝素的分泌,提高NO/ET-1比值,缓解微循环障碍,减轻局部炎症反应。

The concentrations of NO,ET-1,PGI2,TXA2,P-selectin and sICAM-1 which were induced by SLT-Ⅱe in intestinal microvascular endothelial cells of rats were determined to study the functional mechanism of emodin on edema disease of swine.The cultured RIMECs in vitro were divided into control group,SLT-Ⅱe group,test 1 group,test 2 group and test 3 group.The concentrations of NO,ET-1,PGI2,TXA2,P-selectin and sICAM-1 in cell supernatant which were cultivated for 3 h,6 h,9 h and 12 h were detected by ELISA,respectively.In result,10 μg/mL emodin had reduced the secretion of NO,ET-1 and P-selectin remarkably.The secretion of PGI2,TXA2 and sICAM-1 were not reduced by 1 μg/mL,5 μg/mL and 10 μg/mL emodin.In conclusion,emodin could reduce the overfull secretion of NO,ET-1 and P-selectin in IMECs of rat,increase NO/ET-1 ratio,relive intestinal microcirculation obstruction,and alleviate the inflammation response.