达纳康对大鼠溃疡性结肠炎细胞因子的影响  

Effects of Ginkgo biloba extract on cytokines in rats with TNBS-induced ulcerative colitis

作　　者：周燕红[1] 于皆平[1] 何小飞[2] 余细球[1] 

机构地区：[1]武汉大学人民医院消化内科,湖北省武汉市430060 [2]咸宁医学院附属医院消化内科,湖北省咸宁市437100

出　　处：《世界华人消化杂志》2004年第2期371-375,共5页World Chinese Journal of Digestology

摘　　要：目的:观察大鼠实验性溃疡性结肠炎脾淋巴细胞,肠组织和血清中,细胞因子的表达及达纳康对其的影响,探讨达纳康对溃疡性结肠炎的保护作用及其机制.方法:用三硝基苯磺酸(TNBS)建立大鼠溃疡性结肠炎模型.将动物随机分为空白对照组、三硝基苯磺酸、三硝基苯磺酸+生理盐水组、三硝基苯磺酸+达纳康组四组观察肠道大体形态和组织学改变.采用ELISA法测定脾细胞、大肠黏膜及血清中的白介素-12(IL-12)、干扰素γ(IFN-γ)和白介素4(IL-4).结果:与三硝基苯磺酸组比较三硝基苯磺酸+达纳康损伤指数明显下降(2.83±0.94vs5.33±1.50,P<0.01,1.92±0.67vs4.33±0.98,P<0.01).IFN-γ,浓度明显下降.脾细胞:60±21.5vs125.6±14.6,P<0.01大肠黏膜:202.8±49.6vs431.8±57.6,P<0.01血清:8.6±1.4vs13.5±1.7,P<0.01.与模型组比较TNBS组+EGb组IL-4浓度明显升高(脾细胞:11.2±1.3vs6.05±1.5,P<0.01大肠黏膜:10.2±1.9vs6.9±1.4,P<0.0l血清:7.9±1.8vs4.2±1.1,P<0.01).血清IL-12浓度明显下降(8.2±2.2vs25.8±4.8,P<0.01)血清IL-12/IL-4比值下降(1.13±0.49vs6.4±1.8,P<0.01).IFN-γ/IL-4比值明显下降(脾细胞:5.2±2.0vs21.9±4.9,P<0.01,大肠黏膜:20.9±7.97vs65.9±18,P<0.01;血清:1.1±0.3vs3.4±0.8,P<0.01).结论:TNBS诱导的大鼠UC模型是Thl(IL-12)亚型为主的免疫应答反应,EGb通过抑制IL-12,IFN-γ生成,恢复Th1/Th2细胞因子的平衡,发挥对溃疡性结肠炎的保护作用.AIM: To investigate the effects of Ginkgo biloba extract (Egb) on cytokine profile produced by splenocytes, colonic mucosa and serum and to study the main mechanism of EGb in protection of TNBS-induced ulcerative colitis in rats. METHODS: A rat ulcerative colitis model was induced by 2.4.6-trinitrobenzene sulfonic acid (TNBS). All rats were divided into four groups: normal, TNBS, TNBS+NS, and TNBS+EGb. The macroscopical and histological changes of the colon were evaluated. The IL-12, IFN-γ and IL-4 produced by splenocytes, colonic mulosal and serum were analyzed with ELISA. RESULTS: In TNBS+EGb group, the macroscopical and histological scores were significantly lower than those of TNBS group (2.83±0.94 vs 5.33±1.50, P<0.01, 1.92±0.67 vs 4.33±0.98, P<0.01). In the TNBS+EGb group, a lower level of IFN-γ production in splenocytes (60±21.5 vs 125.6±14.6, P<0.01); colonic mucosa (202.8±49.6 vs 431.8±57.6, P<0.01) and serum (8.6±1.4 vs 13.5±1.7, P<0.01) was noticed as compared with TNBS group. In comparison with TNBS group, significantly increased IL-4 was noticed (splenocytes: 11.2±1.3 vs 6.05±1.5,P<0.01; colonic mucosa: 10.2±1.9 vs 6.9±1.4, P<0.01; serum: 7.9±1.8 vs 4.2±1.1, P<0.01) in TNBS+EGb group. IL-12 production by serum in TNBS+EGb group was lower than that of TNBS group (8.2±2.2 vs 25.8±4.8, P <0.01). The ratio of IL-12/IL-4 was lower in TNBS+EGb group compared with TNBS group (serum: 1.13±0.49 vs 6.4±1.8, P<0.01). The ratio of IL-12/IL-4 was lower than that in TNBS+EGb group compared with TNBS group (splenocytes:5.2±2.0 vs 21.9±4.9, P<0.01; colonic mucosa: 20.9±7.97 vs 65.9±18, P<0.01; serum: 1.1±0.3 vs 3.4±0.8, P<0.01). CONCLUSION: TNBS-induced ulceratived colitis is a Thl type dominant (IL-12 overproduction)murine model; EGb has protective effects on ulcerative colitis of rat by suppresses of increased IL-12 and IFIM-γ and maintaines the balance of helper T cell 1 with helper T cell 2.

关 键 词：达纳康 大鼠 溃疡性结肠炎 细胞因子 血清 大肠黏膜 

分 类 号：R574.62[医药卫生—消化系统] R-332[医药卫生—内科学]