灰绿黄堇总生物碱对实验性溃疡性结肠炎的作用研究

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。

The effect of alkaloids of corydalis adunca maxim on experiment ulcerative colitis induced by dextran sulfate sodium

Objective To investigate the effect of alkaloids of corydalis adunca maxim（ACAM） on experimental ulcerative colitis in mice. Methods BALB/C mice of 6 groups were allowed to drink either 4% dex- tran 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 im- munohistochemistry of expressions of NF-KB p65 and intercellular adhesion molecule 1 （ ICAM-1 ） proteins to ob- serve the damage of colon tissues and. possible mechanisms. Results DAI, MPO activity, MDA content and expressions of ICAM-1 and NF-KB 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 con- tent,improved histological changes of colon tissues, blunted the expressions of NF-KB p65 and ICAM-1 proteins, and promoted SOD activity. Conclusion ACAM 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-KB activation and ICAM-1 expression.