Protective effect of staphylococcal nuclease on 2, 4, 6-trinitro-benzene sulfonic acid-induced colitis in mice
10.11665/j.issn.1000-5048.20200211
- VernacularTitle:金黄色葡萄球菌核酸酶对2,4,6-三硝基苯磺酸诱导的小鼠结肠炎的保护作用
- Author:
Tingting ZHANG
1
;
Yinliu MEI
;
Wanfa DONG
;
Jingxun WANG
;
Liang JIN
;
Jie WU
Author Information
1. 中国药科大学生命科学与技术学院微基因药学实验室
- Publication Type:Journal Article
- Keywords:
staphylococcal nuclease;
Lactococcus lactis;
2,4,6-trinitro-benzene sulfonic acid;
neutrophil extracellular traps;
colitis
- From:
Journal of China Pharmaceutical University
2020;51(2):198-205
- CountryChina
- Language:Chinese
-
Abstract:
To explore the improving effect and mechanism of staphylococcal nuclease(SNase)-mediated degradation of neutrophil extracellular traps(NETs)on 2, 4, 6-trinitro-benzene sulfonic acid(TNBS)-induced colitis in mice. The model of colitis in female BALB/c mice was established by intrarectal injection of 2. 5% TNBS solution, and SNase loaded by Lactococcus lactis(L. lactis)were orally administrated for 6 days. To investigate the effect of SNase-mediated degradation of neutrophil extracellular traps on colitis in mice, the experiment was divided into control group, TNBS model group, NZ900 group and L. lactis pCYT: SNase group. The daily body weight, stool consistency and bleeding of mice were observed. The pathological condition of HE in colon group was detected. The activity of MPO and the mRNA expression level of inflammatory cytokines in each group were measured, and the concentration of inflammatory factors in serum was detected. The expression of NETs level marker citH3 in colon tissue was determined by immunohistochemistry. The results showed that SNase loaded by lactis acid bacteria could alleviate the weight loss, disease activity index score, colonic length and pathological damage induced by TNBS in mice, and reduce the levels of inflammatory cytokines in serum and colonic tissue, inhibit the activity of MPO and the expression of Ly6G and citH3 in colon tissue. The preliminary mechanism showed that SNase could down-regulate the expression of inflammatory cytokines and reduce the content of NETs markers to alleviate colitis in mice.
