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作 者:王轩[1] 陈斌[1] 彭杰[1] 苏煦初[1] 孙克伟[1] 李武[1] 周为[1]
机构地区:[1]湖南中医药大学第一附属医国家中医(肝病)临床研究基地,湖南省中医药管理局重型肝炎证治研究室,国家中医药管理局中医肝胆病重点学科,湖南长沙410007
出 处:《中西医结合肝病杂志》2013年第3期157-159,共3页Chinese Journal of Integrated Traditional and Western Medicine on Liver Diseases
基 金:国家中医临床研究基地业务建设科研专项(No.JDZX2012062);湖南省中医药科研基金重点课题(No.201205);湖南省普通高等学校青年骨干教师培养基金(No.2010)
摘 要:目的:动态观察温阳解毒化瘀颗粒对肝衰竭肠源性内毒血症(ITEM)大鼠肠道sIgA的影响。方法:将大鼠随机分为正常组、模型组及温阳解毒化瘀颗粒组(实验组),模型组和实验组大鼠采用D-半乳糖胺(D-gal)腹腔注射,造肝衰竭ITEM模型;正常组大鼠在腹腔注射生理盐水,12小时后处死,余两组分别于造模后12、24小时各取10只大鼠处死,检测各组大鼠门静脉内毒素水平、肠道sIgA水平并观察肝组织病理学变化。结果:模型组大鼠12小时时肠道sIgA下降,与给药前比较P<0.05;24小时时门静脉内毒素水平明显升高,与给药前比较P<0.01;肝组织大面积坏死。实验组大鼠12小时时各项指标较模型组比较,差异无显著性意义;24小时时门静脉内毒素水平较模型组降低(P<0.05);肠道sIgA分泌较模型组增多(P<0.05);肝组织病变减轻。结论:增加肠道sIgA分泌是温阳解毒化瘀颗粒改善ITEM机制之一。Objective: To observe the effect of Wenyang Jiedu Huayu granule on intestinal sIgA in rat with hepatic failure intestinal endotoxemia(ITEM) dynamically.Methods: The rats were randomly divided into 3 groups: normal group,model group,Wenyang Jiedu Huayu group(experimental group).The rat model of hepatic failure ITEM was established by intraperitoneal injection of D-galactosamin(D-gal).The rats of normal group were put to death 12 hours later after intraperitoneal injection,and respectively select 10 rats and put them to death from the rest each group 12 and 24 hours later after being modeled.Then compared the level of portal endotoxin,intestinal sIgA and liver tissue was collected for pathological observation.Results: Intestinal sIgA of model group decreased at 12h(P &lt; 0.05),the level of portal endotoxin increased obviously(P &lt; 0.01),liver pathology showed that a large area of liver tissue became necrosis.Experimental group was not different from model group at 12h,and the level of portal endotoxin was lower than model group at 24h(P &lt; 0.01),intestinal sIgA was increased compared with model group at 24h(P &lt; 0.05).Lesions of liver tissue were smaller.Conclusion: It is the one mechanism of action of improving ITEM that Wenyang Jiedu Huayu granule could increase the intestinal sIgA.
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