Tang Qing, Fan Heng, Shou Zhexing, Liu Xingxing
Union Hospital, Tongji Medical College of Huazhong University of Science and Tecnology, Wuhan 430022, China.
Zhongguo Zhong Yao Za Zhi. 2012 Jun;37(12):1814-7.
To study the effect of NOD2 on colitis pathogenesis in experimental rats, and discuss therapeutical effect and mechanism of kushenin injection (OMT) on colitis in experimental rats.
Fourty Sprague-Dawley (SD) rats were randomly divided into four groups: the normal control group, the model group, the SASP group, and the OMT group, with 10 rats in each group. Except the normal control group, models were established in the remaining three groups with TNBS. The OMT group was injected with kushenin injection, the SASP group was orally administered with mesalazine suspension, the model group and the normal group were orally administered with distilled water for 15 days. Colon lesion score and histological score of experimental rats were observed. Expression of NOD2, NF-kappaB p65 protein in rats colonic mucous was detected by immunohistochemistry. Expression of IL-6 in rat colon mucous was detected by ELISA.
Compared with normal control group, the expression of NOD2, NF-kappaB p65 and IL-6 in colonic mucosa of the model group were significantly increased (P < 0.01). The SASP group and the OMT group showed lower expressions of NOD2, NF-kappaB p65 and IL-6 in colonic mucosa than the model group (P < 0.01, P < 0.05).
The over expression of colonic mucosa proteins NOD2 and NF-kappaB p65 and increasing secretion of IL-6 take part in the appearance and development of ulcerative colitis. OMT can attenuate ulcerative colitis and protect colonic mucosa by inhibiting expression of NOD2, NF-kappaB p65 and decreasing IL-6.
研究NOD2在实验性大鼠结肠炎发病机制中的作用，并探讨苦参素注射液（OMT）对实验性大鼠结肠炎的治疗作用及机制。
将40只Sprague-Dawley（SD）大鼠随机分为四组：正常对照组、模型组、柳氮磺胺吡啶（SASP）组和OMT组，每组10只。除正常对照组外，其余三组用三硝基苯磺酸（TNBS）建立模型。OMT组注射苦参素注射液，SASP组口服美沙拉嗪混悬液，模型组和正常组口服蒸馏水，共15天。观察实验大鼠的结肠病变评分和组织学评分。采用免疫组织化学法检测大鼠结肠黏膜中NOD2、核因子κB p65（NF-κB p65）蛋白的表达。采用酶联免疫吸附测定（ELISA）法检测大鼠结肠黏膜中白细胞介素-6（IL-6）的表达。
与正常对照组相比，模型组结肠黏膜中NOD2、NF-κB p65和IL-6的表达显著升高（P<0.01）。SASP组和OMT组结肠黏膜中NOD2、NF-κB p65和IL-6的表达低于模型组（P<0.01，P<0.05）。
结肠黏膜蛋白NOD2和NF-κB p65的过度表达以及IL-6分泌增加参与了溃疡性结肠炎的发生和发展。OMT可通过抑制NOD2、NF-κB p65的表达及降低IL-6水平减轻溃疡性结肠炎并保护结肠黏膜。
