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目的:探讨溃结康胶囊对TNBS诱导大鼠结肠炎的治疗作用。方法:制备TNBS结肠炎大鼠模型,实验设正常对照组、模型对照组、阳性药物对照组(柳氮磺吡啶, 0. 50g/kg)、溃结康给药组( 0. 64, 0 .32, 0 .16g/kg),采用灌胃方式给药,给药时间从制备模型6d后开始,连续12天。实验结束后观察大鼠结肠粘膜损伤指数(CMDI)、粪便隐血(OB)、髓过氧化物酶(MPO)活性和粘膜病理组织学情况,并检测结肠组织丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH- Px)含量;胸腺、脾脏称重。结果:溃结康可减轻TNBS结肠炎大鼠的CMDI和OB程度,降低MPO水平,可改善结肠粘膜病理损伤;并可明显对抗胸腺萎缩和脾脏肿大;同时溃结康可明显降低MDA含量,增加SOD和GSH- Px水平。结论:溃结康对TNBS诱导的大鼠结肠炎有良好的治疗作用,其机理可能与抗炎、免疫调节和抗氧化损伤有关。
Objective: To investigate the therapeutic effect of Kuijiekang capsule on TNBS-induced colitis in rats. METHODS: A rat model of TNBS colitis was prepared. The experiment was divided into normal control group, model control group, positive drug control group (sulfasalazine, 0. 50g/kg) and Kuijiekang administration group (0.64, 0. 32, 0.16 g/kg) was administered by intragastric administration. The time of administration was 6 days after the preparation of the model and continued for 12 consecutive days. At the end of the experiment, the rats were observed for CMDI, occult occult blood (OB), myeloperoxidase (MPO) activity and mucosal histopathology. Malondialdehyde (MDA) and superoxide were detected in the colon tissue. Dismutase (SOD) and glutathione peroxidase (GSH-Px) levels; thymus and spleen were weighed. Results: Kuijiekang can reduce the degree of CMDI and OB in rats with TNBS colitis, reduce the level of MPO, can improve the mucosal pathological lesions, and can significantly counteract thymus atrophy and splenomegaly; at the same time, Kuijiekang can significantly reduce MDA content. Increase SOD and GSH-Px levels. Conclusion: Kuijiekang has a good therapeutic effect on TNBS-induced colitis in rats, and its mechanism may be related to anti-inflammatory, immune regulation and anti-oxidative damage.