机构地区:[1]福建医科大学附属第一医院消化内科,350005
出 处:《国际消化病杂志》2009年第3期201-204,共4页International Journal of Digestive Diseases
摘 要:目的探讨伴或不伴高脂血症的重症急性胰腺炎(SAP)大鼠的肠道免疫功能改变及可能的机制。方法40只雄性SD大鼠,随机等分为4组:A组(正常对照组);B组(高脂血症组);C组(SAP组);D组(高脂血症+SAP组)。采用高脂饲料喂养4周建立大鼠高脂血症模型,采用逆行胰胆管注射3.5%牛磺胆酸钠制作大鼠SAP模型。建立SAP模型24h后处死动物,临床全自动生化仪检测血清三酰甘油(TG),鲎试剂法检测大鼠门静脉血内毒素水平,免疫组化方法检测小肠黏膜组织CD4+、CD8+T淋巴细胞数量,免疫放射分析法测定肠黏膜组织中分泌型免疫球蛋白A(sIgA)含量,分光光度计法测定肠道谷氨酰胺(Gln)摄取率、肠黏膜Gln含量、谷氨酰胺酶(GA)活力。结果B组血清TG值均较A组明显升高(P<0.01),D组血清TG值均较C组明显升高(P<0.01);C组血内毒素水平显著高于A组(P<0.01),小肠黏膜组织CD4+、CD8+T淋巴细胞数量、sIgA含量、肠道Gln摄取率、肠黏膜Gln含量、GA活力较A组显著降低(P<0.05~P<0.01);D组血内毒素水平较C组明显升高(P<0.01),小肠黏膜组织CD4+、CD8+T淋巴细胞数量、sIgA含量、肠道Gln摄取率、肠黏膜Gln含量、GA活力较C组显著降低(P<0.05~P<0.01)。结论SAP早期即出现肠道免疫功能受损,肠黏膜Gln代谢改变可能在这一损伤过程中起重要作用;高脂血症可加重SAP大鼠肠道免疫功能受损,而肠黏膜Gln代谢改变可能是高脂血症加重SAP肠道免疫功能受损的机制之一。Objective To explore the change of intestinal immune function in severe acute pancreatitis in rats with and without hyperlipidemia and its possible mechanisms.Methods A total of 40 male SD rats were randomly divided into 4 groups:group A(control group),group B(group of hyperlipemia),group C(group of SAP),group D(group of hyperlipemia+SAP).Hyperlipemia rat model was established by feeding a high-fat diet for 4 weeks.SAP rat model was established by retrograde injection of 3.5% sodium taurocholate into the biliopancreatic duct.Rats were sacrificed at 24 hours after models were made;the concentration of TG in serum was measured by clinical automatic biochemical analyzer,endotoxin concentration in portal vein was determined by limulus methods;CD4+,CD8+T lymphocytes in intestinal mucosa were examined by immunohistochemistry;the sIgA contents of intestinal mucosa was examined by radioimmunoassay;the glutamine uptake rate,concentration of glutamine and activity of GA in intestinal mucosa was examined by using spectrophotometry.Results The serum TG value in the group B was higher than that in the group A(P<0.01).The serum TG value in the group D was higher than that in the group C(P<0.01).Compared to the group A,plasma endotoxin concentration in the portal vein increased,and the levels of CD4+,CD8+T lymphocyte,sIgA,glutamine uptake rate,glutamine and activity of GA in the intestinal mucosa reduced significantly in the group C(P<0.05~P<0.01);Compared to the group C,the group D had a higher level of plasma endotoxin concentration in the portal vein and lower levels of CD4+,CD8+T lymphocyte,sIgA,glutamine uptake rate,glutamine and activity of GA in the intestinal mucosa(P<0.05~P<0.01).Conclusions Intestinal immune suppression occurred in the early stage of SAP.Hyperlipemia can make SAP more serious through intestinal immune suppression way,and the change of glutamine metabolism in the intestinal mucosa may play an important role.
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