【摘要】 目的研究灰绿黄堇总生物碱(ACAM)对小鼠结肠炎的作用及其机制。方法实验设正常、模型、柳氮磺胺吡啶组(SASP,520mg/kg)和ACAM组(100、200、400mg/kg)。正常组小鼠饮用蒸馏水,其余组自由饮用4%葡聚糖硫酸钠(DSS)水溶液,同时分别灌胃给予溶剂或干预药物(0.2ml/10g,1次/d×7d)。记录小鼠疾病活动指数(DAI);测定结肠组织MDA含量,SOD、MPO活性及ICAM-1、NF-κBp65表达水平。结果模型组DAI显著增高,结肠黏膜损伤严重;MDA舍量、MPO活性及ICAM-1和NF-κBp65表达明显升高。SOD活性下降(P<0.01)。SASP520mg/kg能明显逆转上述改变;ACAM100mg具有相似的作用。结论ACAM可能通过抗氧自由基作用,抑制炎性细胞活化、迁移及NF-κB激活,缓解小鼠结肠炎性反应。更多还原

【Abstract】 Objective To investigate the effect of alkaloids of corydalis adunca maxim(ACAM)on experimental ulcerative colitis in mice.MethodsBALB/C mice of 6 groups were allowed to drink either 4%dextran sulfate sodium(DSS)solution or distilled water freely with different doses of ACAM(50,100,200 mg/kg)or salicylazosulfapyridine(SASP,520 mg/kg),and solvent(0.2 ml/10 g)once a day for 7 days,respectively.The symptom of ulcerative colitis was evaluated by disease activity index(DAI),Myeloperoxidase(MPO)and superoxide dismutase(SOD)activities and malondialdehyde(MDA)content were determined by HE staining and immunohistochemistry of expressions of NF-κB p65 and intercellular adhesion molecule 1(ICAM-1)proteins to observe the damage of colon tissues and.possible mechanisms.ResultsDAI,MPO activity,MDA content and expressions of ICAM-1 and NF-κB were markedly increased,while SOD activity decreased in DSS-treated mice.Treatment of different doses of ACAM or SASP in mice decreased significantly DAI,MPO activity and MDA content,improved histological changes of colon tissues,blunted the expressions of NF-κB p65 and ICAM-1 proteins,and promoted SOD activity.ConclusionACAM has excellent therapeutic effect on ulcerative colitis caused by DSS.The possible mechanism may be related to its antioxidant and anti-inflammatory activities associated with inhibiting the NF-κB activation and ICAM-1 expression.更多还原