Monotropein alleviates secondary liver injury in chronic colitis by regulating TLR4/NF-κB signaling and NLRP3 inflammasome

被引:40
作者
Chen, Yonger [1 ]
Lu, Yingyu [1 ,2 ]
Pei, Chaoying [1 ]
Liang, Jian [2 ]
Ding, Ping [1 ,2 ]
Chen, Shuxian [1 ,3 ]
Hou, Shao-Zhen [1 ,2 ]
机构
[1] Guangzhou Univ Chinese Med, Sch Pharmaceut Sci, Guangzhou 510006, Guangdong, Peoples R China
[2] Guangzhou Univ Chinese Med, Math Engn Acad Chinese Med, Guangdong Prov Key Lab New Drug Dev & Res Chinese, Guangzhou 510006, Guangdong, Peoples R China
[3] Sun Yat Sen Univ, Affiliated Hosp 3, Guangzhou 510000, Guangdong, Peoples R China
关键词
Monotropein; DSS; Secondary liver injury; TLR4/NF-kappa B; NLRP3; ACTIVATION; STEATOHEPATITIS; MECHANISMS; EXPRESSION; ACID;
D O I
10.1016/j.ejphar.2020.173358
中图分类号
R9 [药学];
学科分类号
100702 [药剂学];
摘要
Recently, it has reported that many inflammatory bowel disease (IBD) patients were contracted secondary liver injury. Monotropein (MON), an iridoid glycoside, is demonstrated to possess protective effects on acute colitis mice due to its anti-inflammatory activities. However, it was remained unknown whether MON could inhibit secondary liver injury caused by IBD. The aim of the present study was to investigate the protective roles and mechanisms of MON on secondary liver injury in chronic colitis mice model. In this study, 2% Dextran sodium sulfate (DSS) was used to induce mice model of chronic colitis. The results showed that MON attenuated DSS-induced hepatic pathological damage, liver parameters, infiltration of macrophages and cytokines levels. Furthermore, we found that MON attenuated liver injury through suppressing the activation of the toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-kappa B) signaling pathway and down-regulating the activity of NLRP3 (NOD-, LRR- and pyrin domain-containing 3) inflammasome. All the data indicated that MON may be an effective therapeutic reagent to attenuate secondary liver injury induced by chronic colitis.
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页数:8
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