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目的:观察黄芩苷对三硝基苯磺酸(TNBS)致小鼠实验性结肠炎的保护作用,并探讨其作用机制。方法:将Balb/c小鼠分为4组:乙醇对照组、TNBS模型组、黄芩苷低剂量组和黄芩苷高剂量组。用TNBS灌肠诱导小鼠实验性结肠炎模型,TNBS灌肠2h后,灌胃给予黄芩苷,qd×7d。第8天处死动物,观察结肠黏膜的损伤程度,测定结肠髓过氧化物酶(MPO)活性以及丙二醛(MDA)和谷胱苷肽(GSH)的含量。结果:与TNBS模型组比较,黄芩苷低、高剂量组小鼠体质量、大体损伤评分及组织学表现均显著改善,MPO酶活性显著降低,MDA含量减少,谷胱苷肽含量增加。结论:黄芩苷可减轻TNBS诱导的小鼠实验性结肠炎,作用机制与黄芩苷的抗氧化作用有关。
Objective: To observe the protective effect of baicalin on experimental colitis induced by trinitrobenzene sulfonic acid (TNBS) in mice and its mechanism of action. Methods: Balb / c mice were divided into 4 groups: ethanol control group, TNBS model group, low dose baicalin group and high dose baicalin group. TNBS enema induced experimental colitis model in mice, TNBS enema 2h, intragastric administration of baicalin, qd × 7d. The animals were sacrificed on the 8th day to observe the degree of colonic mucosal injury. The activity of colonic myeloperoxidase (MPO) and the content of malondialdehyde (MDA) and glutathione (GSH) were determined. Results: Compared with TNBS model group, the body weight, gross lesion score and histological appearance of mice in low and high dose baicalin groups were significantly improved, the activity of MPO enzyme, the content of MDA and the content of glutathione increased significantly. CONCLUSION: Baicalin can relieve experimental colitis induced by TNBS in mice and the mechanism of action is related to the anti-oxidative effect of baicalin.