黄芪多糖对三硝基苯磺酸诱导溃疡性结肠炎大鼠的保护作用

本研究探讨黄芪多糖(APS)对2,4,6-三硝基苯磺酸(TNBS)诱导溃疡性结肠炎(UC)大鼠的保护作用。将72只SD大鼠随机分为正常组、模型组、柳氮磺胺吡啶(SASP)阳性组、APS低、中、高剂量组(100、200、400mg·kg-1),每组12只,除正常组外,每组以150mg·kg-1 TNBS乙醇溶液灌肠制备大鼠结肠炎模型。造模24h后,SASP阳性组及黄芪多糖组分别给予相应的药物进行灌胃干预,每日1次,连续给药14d。研究过程中观察大鼠体重、评价其活动指数(DAI)及结肠黏膜损伤(CMDI),并于给药结束后检测大鼠血清和组织中的炎症因子及生化指标。结果表明,黄芪多糖可以显著改善UC大鼠活动指数,减轻大鼠黏膜损伤,且APS高剂量组大鼠组织中丙二醛(MDA)、髓过氧化物酶(MPO)水平相比模型对照组显著降低,超氧化物歧化酶(SOD)水平显著增加(p<0.05);同时血清中炎症因子TNF-α、IL-6含量相比模型对照组显著降低,IL-10含量显著增加(p<0.05)。因此,黄芪多糖对TNBS诱导的大鼠溃疡性结肠炎具有一定的保护作用。

Protective Effects of Astragalus Polysaccharide on Ulcerative Colitis Rats Induced by Trinitrobenzene Sulfonic Acid

To investigate the protective effects of astragalus polysaccharides(APS)on ulcerative colitis(UC)rats induced by 2,4,6-trinitrobenzene sulfonic acid(TNBS),72 SD rats were randomly divided into normal group,model group,sulfasalazine(SASP)positive group and low,medium and high dose of APS groups(100mg·kg-1,200mg·kg-1,400mg·kg-1),12 rats in each group.Except the normal group,rats in other groups were prepared by 150mg·kg-1 TNBS ethanol solution as colitis model.24 hours after modeling,the positive group and APS group were given corresponding drugs for oral administration,once a day,for 14 days successively.In the course of the study,the rat weight,evaluating the activity index(DAI)and the colonic mucosal damage(CMDI)were observated,and the inflammatory factors and biochemical indexes in serum and tissue of rats were performed.The results show that the APS could significantly improve the UC rat activity index,reduce the colonic mucosal damage.Compared with the model control,the levels of malondialdehyde(MDA)and myeloperoxidase(MPO)in the tissue of the APS high dose group decreased significantly,superoxide dismutase(SOD)level increased significantly(p<0.05).Meanwhile the serum inflammatory tumor necrosis factor content in the APS high dose group compared to model control group,the TNF-a,IL-6contents were decreased and the IL-10 content increased(p<0.05).Therefore,APS has protective effect on ulcerative colitis induced by TNBS in rats.