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目的:观察核因子κB必需分子(NEMO)结合的小分子多肽(NBD多肽)对实验性大鼠溃疡性结肠炎治疗作用的时效关系。方法:64只SD大鼠随机分成3d组、7d组,采用三硝基苯磺酸(TNBS)灌肠法制作溃疡性结肠炎大鼠模型,予腹腔注射1.3mg/100g NBD多肽评估炎症活动指数(IAI)评分,按照给药后3,7d分别处死各组的动物取结肠,肉眼观察结肠黏膜病变且按损伤情况积分,行病理切片、苏木素伊红(hematoxylin eosin,HE)染色,光镜下评估组织损伤,取病变结肠组织切片行免疫组化检测核因子κB(NF-κB)表达,其上清用相应试剂盒检测髓过氧化物酶(MPO)、丙二醛(MDA)。结果:7d组组织学损伤评分、IAI评分分别为(4.8±0.8)、(3.0±0.5),明显低于3d组(6.9±0.7)、(5.1±0.6)(P<0.05);7d组MDA、MPO及NFκ-B表达的阳性细胞百分率、平均光密度值为[(3.8±0.5)、(2.2±0.4)、(21.3±3.5)%、(51.1±2.9)],均少于3d组[(5.1±0.8)、(3.4±0.5)、(52.1±2.4)%、(65.4±3.4)](P<0.05)。结论:NBD多肽对于溃疡性结肠炎大鼠模型有较好的治疗作用,随着时间的延长,疗效逐渐增强,其作用与其抑制NFκ-B表达有关。
Objective: To observe the effect of NEMO binding small molecule peptide (NBD polypeptide) on the therapeutic effect of ulcerative colitis in experimental rats. Methods: Sixty-four Sprague-Dawley rats were randomly divided into 3d and 7d groups. The rat model of ulcerative colitis was established by TNBS enema, and the inflammatory activity index ( (IAI). The animals in each group were sacrificed on the 3rd and 7th day after the administration, and the colonic mucosa lesions were observed by naked eyes. The pathological sections were taken according to the injury scores. The hematoxylin eosin (HE) staining and light microscopic evaluation Tissues were harvested for histological examination. The expression of nuclear factor kappa B (NF-κB) was detected by immunohistochemistry in the sections of diseased colon. The supernatants were tested for myeloperoxidase (MPO) and malondialdehyde (MDA) using the corresponding kit. Results: The scores of histological injury and IAI in 7d group were (4.8 ± 0.8) and (3.0 ± 0.5) respectively, significantly lower than those in 3d group (6.9 ± 0.7 and 5.1 ± 0.6, P <0.05) , The percentage of positive cells expressing MPO and NFκ-B were (3.8 ± 0.5), (2.2 ± 0.4), (21.3 ± 3.5)%, (51.1 ± 2.9) (5.1 ± 0.8), (3.4 ± 0.5), (52.1 ± 2.4)%, (65.4 ± 3.4)] (P <0.05). CONCLUSION: NBD peptide has a good therapeutic effect on the rat model of ulcerative colitis. With the prolongation of time, the efficacy of NBD peptide gradually increases, which is related to the inhibition of NFκB expression.