首页> 中文期刊> 《中国中医急症》 >连术颗粒对内毒素血症大鼠肠黏膜免疫功能的影响

连术颗粒对内毒素血症大鼠肠黏膜免疫功能的影响

         

摘要

目的 探讨连术颗粒对内毒素血症大鼠肠道黏膜免疫功能的保护作用.方法 将健康SD大鼠随机分为正常对照组、模型组、连术颗粒组(1.8 g/kg)、黄连素组(0.2 g/kg),每组10只,灌服相应药物,疗程72 h.疗程结束后,除正常对照组外,每只腹腔注射脂多糖(LPS)30 mg/kg,观察大鼠一般情况;收集小肠黏膜,HE染色观察肠道黏膜改变、采用放射免疫法检测肠道黏膜TNF-α、IL-1β、SIgA含量改变、免疫组化法检测小肠IgA+浆细胞数量、MTT法检测淋巴细胞(T、B细胞)增殖活力.结果 与正常组相比,模型大鼠腹泻次数明显增加,肠黏膜可见明显病理性改变,且T、B淋巴细胞增殖抑制,TNF-α、IL-1β炎症因子大量分泌,肠道免疫功能受损,即SIgA含量、IgA+浆细胞数量减少.连术颗粒在促进肠道T、B淋巴细胞增殖、SIgA含量,增加IgA+浆细胞数量,减少TNF-α、IL-1β炎症因子分泌方面均优于黄连素组.结论 连术颗粒能有效保护内毒素血症大鼠肠黏膜的免疫屏障,其机制可能是促进肠道T、B淋巴细胞增殖、SIgA分泌,减少TNF-α、IL-1β炎症因子释放等.%Objective: To investigate the immune function of Lianshu Particles on intestinal mucosal. Methods: Forty SD rats were divided randomly into four groups;normal group,model group,Lianshu group (1.8 g/kg-1) ,and Berberine group(0.2 g/kg-1)- 10 each,fed with different drugs,treatment for 72 hours. After the treatment,in addition to the normal group, each injected LPS 30 mg/kg"1. Observed the performance of rats; Observed intestinal mucosal changes by HE staining;TNF-α,IL-lp,SIgA was detection by radioimmunoassay;the number of intestinal IgA + plasma cell was measured by Immunohistochemical staining;The proliferative activtity of lympholytes in intestinal mucosal intraepithelial tissues was assessed by MTT colorimetric assays. Result: Compared with normal group,model rats had a significantly increased number of diarrhea,obvious pathological changes in intestinal,besides, T,B lymphocyte proliferation was inhibited,Release large amounts of TNF-α,IL-1β,SIgA concentration, IgA + plasma cells decreased. Lianshu Particles in the promotion of intestinal T,B lymphocyte proliferation,SIgA levels,increasing the number of IgA + plasma cells,reducing TNF-α,IL-1β cytokines were better than berberine group. Conclusion: Endotoxemia can induce local mucosal immune function disorder. Lianshu Particles can effectively protect the intestinal mucosa of endotoxemic rats immune barrier. The mechanism may be the promotion of intestinal T,B lymphocyte proliferation,SIgA secretion,reducing TNF-α,IL-lβ release.

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