Anti-inflammatory effect of recombinant human kallistatin in ulcerative colitis of mice
10.16438/j.0513-4870.2015-1167
- VernacularTitle:重组人组织激肽释放酶结合蛋白对小鼠溃疡性结肠炎的抗炎作用
- Author:
Chen-na ZHENG
1
;
Xun-wei DUAN
2
;
Dong-fang JIA
1
;
Cai-lin LUO
1
;
Ning-qing WANG
3
;
Hui-yong YANG
4
;
Yong DIAO
4
Author Information
1. Quanzhou Medical College, Quanzhou 362000, China
2. Quanzhou Normal University, Quanzhou 362000, China
3. Hainan Weikang Pharmaceutical(Qianshan) Co., Ltd., Qianshan 246300, China
4. School of Biomedical Sciences, Huaqiao University, Quanzhou 362000, China
- Publication Type:ORIGINAL ARTICLES
- Keywords:
kallistatin;
ulcerative colitis;
cytokine;
antioxidation;
tumor necrosis factor- α;
interleukin-10
- From:
Acta Pharmaceutica Sinica
2016;51(7):1077-
- CountryChina
- Language:Chinese
-
Abstract:
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.