甘露糖结合凝集素在小鼠葡聚糖硫酸钠结肠炎发病中的机制研究

Mannose-binding lectin and dextran sodium sulfate-induced colitis in mice

目的甘露糖结合凝集素(Mannan-binding lectin,MBL)可与甘露糖相关丝氨酸蛋白酶(MBL-associated serineproteases,MASP)结合激活补体系统级联反应。文中检测葡聚糖硫酸钠(dextran sulfate sodium,DSS)诱导小鼠急性肠炎的血清MBL与MASP表达水平,以及在糖皮质激素治疗后两者的表达情况。方法将40只8周龄Balb/c小鼠随机分为正常组、模型组、治疗组和对照组,每组10只小鼠。自由饮用5%DSS溶液7 d,造成急性溃疡性结肠炎(ulcerative colitis,UC)模型。小鼠腹腔麻醉后取主动脉血,并立即分离血清,用ELISA方法检测其MBL与MASP的浓度。结果DSS诱导肠炎中MBL与MASP的表达明显高于正常组。用糖皮质激素治疗后MBL的水平明显下降,但MASP的水平变化无统计学意义。结论在5%DSS溶液诱导的小鼠急性溃疡性结肠炎模型中,MBL与MASP相关信号通路的活化可能参与了UC的发病与进展。糖皮质激素抑制了MBL的产生,可能与其对UC的治疗有关,而与MASP无关。

Objective Mannose-binding lectin （MBL） circulates in association with a group of MBL-associated serine proteases （MASP）. This combination leads to the complement pathway. We aimed to investigate the expressions of MBL and MASP in the serum of the mice with acute colitis induced by dextran sulfate sodium （DSS） in comparison with their expressions after prednisolone treatment. Methods Forty 8-week-old BALB/c mice were equally randomized into 4 groups, normal, model, treatment and control. Ulcerative colitis （UC） models were made by feeding the mice on 5% DSS solution for 7 days. The normal and model mice were sacrificed on day 7, and the others on day 14, for the measurement of the length and weight of the colons. The levels of serum MBL and MASP were detected by ELISA. Results The expressions of MBL and MASP in the serum were obviously higher in the DSS-induced colitis models than in the normal controls. After prednisolone treatment, the former was decreased markedly, while the latter showed no statistically significant change. Conclusion MBL and MASP may participate in the development and aggravation of UC. Prednisolone can suppress the production of MBL and play a protective role in the lectin pathway.