Research Papers:

Huaier aqueous extract protects against dextran sulfate sodium-induced experimental colitis in mice by inhibiting NLRP3 inflammasome activation

Lijuan Wang, Zhongxia Yu, Chao Wei, Li Zhang, Hui Song, Bing Chen and Qifeng Yang _

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Oncotarget. 2017; 8:32937-32945. https://doi.org/10.18632/oncotarget.16513

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Lijuan Wang1,*, Zhongxia Yu2,*, Chao Wei3,*, Li Zhang1,4, Hui Song2, Bing Chen1, Qifeng Yang1,4

1Pathology Tissue Bank, Qilu Hospital, Shandong University, Jinan, Shandong 250012, China

2Department of Immunology and Key Laboratory of Infection and Immunity of Shandong Province, Shandong University School of Medicine, Jinan, Shandong 250012, China

3Department of Ophthalmology, Second Hospital of Shandong University, Jinan, Shandong 250033, China

4Department of Breast Surgery, Qilu Hospital, Shandong University, Jinan, Shandong 250012, China

*These authors contributed equally to this work

Correspondence to:

Qifeng Yang, email: [email protected]

Keywords: Huaier, colitis, NLRP3, inflammasome, IL-1β

Received: September 30, 2016     Accepted: March 15, 2017     Published: March 23, 2017


The use of Trametes robiniophila Murr. (Huaier) as a complementary therapy for cancer has recently become increasingly common in China. However, whether Huaier can regulate host immune responses, especially innate immunity, remains largely unknown. The NLRP3 inflammasome is a multimeric complex consisting of NLRP3, ASC and caspase-1. NLRP3 inflammasomes respond to a variety of endogenous (damage-associated molecular patterns) and exogenous (pathogen-associated molecular patterns) stimuli, and play crucial roles in host defense against pathogens and multiple diseases such as ulcerative colitis (UC). In this study, we investigated the anti-inflammatory effect of Huaier in dextran sulfate sodium (DSS)-induced murine colitis and revealed the underlying mechanisms by targeting NLRP3 inflammasomes. In C57BL/6 mice, oral administration of Huaier attenuated DSS-induced colon shortening and colonic pathological damage. Furthermore, we analyzed the effect of Huaier on NLRP3 inflammasome activation in macrophages. Huaier inhibited NLRP3 inflammasome activation-induced IL-1β secretion and caspase-1 cleavage. Moreover, Huaier decreased NLRP3 protein expression via promoting NLRP3 degradation through the autophagy lysosome pathway. Therefore, our findings demonstrate a novel function for Huaier in the regulation of NLRP3 inflammasome activation and suggest a potential role for Huaier in NLRP3 inflammasome-associated diseases.

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