Format

Send to

Choose Destination
See comment in PubMed Commons below
Int Immunopharmacol. 2016 Jun;35:119-26. doi: 10.1016/j.intimp.2016.03.030. Epub 2016 Apr 16.

Baicalin ameliorates experimental inflammatory bowel disease through polarization of macrophages to an M2 phenotype.

Author information

1
Department of Immunology, Mudanjiang Medical College, Mudanjiang, China.
2
Department of Pathology, Mudanjiang Medical College, Mudanjiang, China.
3
Department of Histoembryology, Mudanjiang Medical College, Mudanjiang, China.
4
Department of Laboratory Animals, Mudanjiang Medical College, Mudanjiang, China.
5
Department of Immunology, Mudanjiang Medical College, Mudanjiang, China. Electronic address: xiaodongzhu@126.com.
6
Department of Immunology, Mudanjiang Medical College, Mudanjiang, China. Electronic address: xiaoli2595@126.com.

Abstract

Inflammatory bowel diseases (IBDs) are chronic inflammatory disorders of the intestinal tract. Baicalin, originally isolated from the root of the Chinese herb Huangqin (Scutellaria baicalensis Georgi) and its main active ingredient, has a protective effect against inflammatory responses in several diseases. The present study investigated the effects of baicalin on macrophage polarization and its therapeutic role in IBD. Murine peritoneal macrophages and mice with colitis were treated with baicalin. Macrophage subset distribution, M1 and M2 macrophage-associated mRNA expression, and interferon regulatory factor 4 and 5 (IRF4 and IRF5) expression were analyzed. siRNA transfection into mouse peritoneal macrophages was utilized to suppress IRF4. Fluorescence-activated cell sorting, western blot, and real-time PCR analyses were performed. Baicalin (50μM) limited lipopolysaccharide (LPS)-induced M1 macrophage polarization; decreased LPS-induced tumor necrosis factor α, interleukin (IL)-23, and IRF5 expression; and increased IL-10, arginase-1 (Arg-1), and IRF4 expression. siRNA-mediated IRF4 silencing significantly impaired baicalin activity. Furthermore, pretreatment with baicalin (100mg/kg) in mice with dextran sodium sulfate (DSS)-induced colitis ameliorated the severity of colitis and significantly decreased the disease activity index (baicalin group, 3.33±0.52 vs. DSS group, 5.67±1.03). Baicalin (100mg/kg) also repressed IRF5 protein expression and promoted IRF4 protein expression in the lamina propria mononuclear cells, and induced macrophage polarization to the M2 phenotype. In summary, our results showed that baicalin upregulates IRF4 protein expression and reverses LPS-induced macrophage subset redistribution. Thus, baicalin alleviates DSS-induced colitis by modulating macrophage polarization to the M2 phenotype.

KEYWORDS:

Baicalin; Colitis; IRF4; IRF5; M2 macrophage

PMID:
27039210
DOI:
10.1016/j.intimp.2016.03.030
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center