二硝基氯苯致敏溃疡性结肠炎大鼠细胞因子活性研究

Effect of 2,4-dinitrobenzene-1-chlorobenzene in ulcerative colitis rats

目的:探讨二硝基氯苯(DNCB)致敏联合醋酸灌肠法对溃疡性结肠炎(UC)模型大鼠细胞因子的影响。方法:采用二硝基氯苯致敏联合醋酸灌肠法及醋酸灌肠法对SD大鼠进行溃疡性结肠炎造模,并做对比研究。SD大鼠随机分为复合造模组、醋酸造模组、空白对照组。空白组作为各项指标对照,各组均予生理盐水灌胃治疗,分别在第1、15和29d取样观测大鼠的一般情况变化、结肠组织黏膜损伤评分(CMDI)、病理组织学评分(TDI),检测血清IL-2、IL-4、IL-6、IL-10、IL-17、IL-23等细胞因子水平,并对各组细胞因子与黏膜评分及病理评分进行相关性比较。结果:IL-2:与对照组比较,复合组(第1 d、第15 d)和醋酸组(第1 d)显著降低;而复合组第15 d与醋酸组第15 d比较显著降低。IL-6:与对照组及醋酸组(第1 d)比较,复合组(第1 d)显著升高。IL-10:与对照组比较,复合组(第1 d、第15 d)和醋酸组(第1d、第15 d、第29 d)显著降低;IL-17:与对照组比较,复合组(第1 d、第15 d)和醋酸组(第1 d)显著降低;而醋酸组(第15d)与复合组(第15 d)比较显著升高。CMDI:与对照组比较,各组均有显著升高。TDI:与对照组比较,醋酸(第1 d)、复合(第1 d)有显著升高。相关性:IL-2、IL-10、IL-17与CMDI明显相关;IL-2与TDI明显相关。结论:二硝基氯苯致敏联合醋酸灌肠法及醋酸灌肠法均能造成SD大鼠溃疡性结肠炎,与醋酸灌肠法比较,二硝基氯苯致敏联合醋酸灌肠法有可能通过下调IL-2,上调IL-6、IL-17,从而加重和延长大鼠免疫紊乱的状态。

Objective： To observe therapeutic effect and mechanism of 2,4 -dinitrobenzene - 1 - chlorobenzene（DNCB） in rat ulcerative colitis （ UC ） model. Method： 78 SD rats were randomly divided into 3 groups ： normal control （ n = 10） , DNCB UC model （ n = 35 ） , acetic UC model （ n = 33 ）. The rats of DNCB UC model group was established by an enema of DNCB and acetic acid. The rats of acetic UC model group was established by an enema of acetic acid. The rats were sampled in batches when 1 d, 15 d and 29 d. the colon mucosal damage index （CMDI） and tissuedamage index （TDI） were evaluated, the serum levels of interleukin -2 （ IL - 2）, IL - 4, IL - 6, IL - 10, IL - 17 and IL - 23were determined by enzyme - linked immunosor - bant assay （ELISA）. The descriptive and correlational analyses were conducted. Results： Compared with normal control group, DNCB UC model（ 1 d, 15 d） IL -2 declined significantly, IL - 17 increased significantly. Compared with DNCB UC model（ 15 d）, acetic UC model（ 15 d） IL - 2 increased significantly, IL- 17 declined significantly. Compared with normal control group, DNCB UC model IL- 6 increased significantly. Compared with normal control group, DNCB UC model（ 1 d, 15 d） and acetic UC model（ 1 d, 15 d,29 d） IL- 10 declined significantly. Compared with normal control group, both CMDI and TDI were increased significantly in DNCB UC model and acetic UC model. Conclusion： Immune dysfunction is one of causes resulting in colonic inflammatory damage by enema of DNCB and acetic acid. These occurrences are intimatly related to cytokine level of IL- 2, IL- 6, IL- 10, IL- 17.