摘要
本文考察了重组人组织激肽释放酶结合蛋白(kallistatin,Kal)对溃疡性结肠炎(UC)小鼠模型的体内抗炎效果。采用4%葡聚糖酸钠(DSS)建立小鼠UC模型,随机分为模型组与Kal高、中、低剂量治疗组及柳氮磺胺吡啶(SASP)治疗组,并与正常对照组比较。测定6组间小鼠体重、结肠长度及病变组织炎症因子及IL-10和TNF-α水平变化,并进行组织损伤评分。结果显示,与模型组相比,Kal高剂量治疗组和SASP治疗组的组织损伤评分、MPO/MDA/TNF-α水平均显著降低,而小鼠体重、IL-10水平和SOD活性则显著提高,趋近于正常对照组,经过Kal治疗后小鼠溃疡性结肠炎得到了明显的改善,且呈剂量依赖性。因此,本研究揭示了Kal可以改善小鼠溃疡性结肠炎,可能与其参与调控炎性细胞因子IL-10、TNF-α水平及具有一定抗氧化能力有关。
This study was designed to evaluate the anti-inflammatory effect of recombinant human kallistatin（Kal） on ulcerative colitis（UC） in the mouse model. Acute colitis was induced by administration of 4% dextran sodium suffate（DSS） to KM mice for 7 days. The mice were then randomized into 5 groups： model control, Kal 0.2 mg·kg^-1·d^-1, 1.0 mg·kg^-1·d^-1 and 2.0 mg·kg^-1·d^-1 group, salazosulfapyridine（SASP） group. Ten age-matched normal KM mouse were administered with saline in the normal control. The weight, colon length, inflammation factor（MPO/SOD/MDA） and TNF-α/IL-10 levels among the five groups of mice were determined. The results showed that histological index score and MPO/MDA/TNF-α levels of high-dose Kal treatment group and SASP group were significantly lower compared with the model group（P〈0.01）, but the weight, colon length, IL-10 level and SOD activity were significant higher than the model group（P〈0.01）, approaching the normal group. These parameters showed that Kal can significantly relieve the UC state in a dose-dependent manner. This study demonstrates that Kal significantly remits UC in mice, and participates in the regulation of inflammatory cytokines TNF-α/IL-10 levels and has some antioxidant activity.
出处
《药学学报》
CAS
CSCD
北大核心
2016年第7期1077-1082,共6页
Acta Pharmaceutica Sinica
基金
国家自然科学基金青年项目(81502687)
福建省自然科学基金项目(2015J01138
2016J01420)
福建省卫生厅青年科研课题(2012-2-118)
