次级淋巴组织趋化因子在溃疡性结肠炎发病中的作用

目的 探讨次级淋巴组织趋化因子(SLC)对实验性溃疡性结肠炎(UC)大鼠结肠病变的影响.方法 60只SD大鼠随机分为对照组、UC模型组(模型组)及SLC抗体干预治疗UC模型组(干预组),观察、比较不同组别结肠黏膜炎性和淋巴细胞归巢状况以及结肠组织细胞因子(IL-2和IL-6)的变化.逆转录聚合酶链反应(RT-PCR)半定量法检测结肠组织中的SLC表达.结果 3组大鼠的结肠黏膜炎性反应评分和结肠组织细胞因子含量差异有统计学意义(P<0.05和P<0.01).模型组和干预组的结肠黏膜下存在淋巴细胞异常归巢现象;模型组和干预组SLCmRNA的表达量比对照组明显升高(0.846+0.047和0.768±0.135比0.312±0.112,P<0.01),但模型组与干预组间比较差异无统计学意义(P>0.05).结论 SLC与实验性溃疡性结肠炎大鼠的结肠黏膜炎性反应密切相关,阻断SLC是减轻结肠黏膜炎性反应的有效途径之一.

Role of secondary lymphoid tissue chemokine in the pathogenesis of rat ulcerative colitis

Objective To investigate the effect of secondary lymphoid tissue chemokine (SLC) on experimental colon lesions in rats with ulcerative colitis. Methods Sixty Spague-Dawley rats were randomly divided into control group, model group and SLC intervention group. Colonic mueosal lesions of different groups were observed with HE staining for inflammation and lymphocyte homing situation. Cytokine IL-2 and IL-6 levels were measured by ABC-ELISA. Semi-quantitative RT-PCR was used to examine the colonic SLC expression. Results Intestinal inflammation score and colonic cytokine levels were significantly different among three groups (P<0.05, P<0.01). Abnormal lymphocyte homing phenomenon under colonic mucosa was found in the model group and the intervention group. SLC mRNA expression of the model and intervention groups increased significantly compared with the control group(0.846±0.047, 0.768±0.135 vs 0.312±0.112, P<0.01). However, there was no significant difference between model group and intervention group. Conclusions SLC may play an important role in experimental colonic mucosal inflammation in rats with ulcerative colitis. Blockade of SLC may be one of effective ways in reducing colonic mucosal inflammation.