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Review
. 2019 May 27;20(10):2588.
doi: 10.3390/ijms20102588.

The Anti-inflammatory Effects of Dietary Anthocyanins against Ulcerative Colitis

Affiliations
Review

The Anti-inflammatory Effects of Dietary Anthocyanins against Ulcerative Colitis

Shiyu Li et al. Int J Mol Sci. .

Abstract

Ulcerative colitis (UC), which is a major form of inflammatory bowel disease (IBD), is a chronic relapsing disorder of the gastrointestinal tract affecting millions of people worldwide. Alternative natural therapies, including dietary changes, are being investigated to manage or treat UC since current treatment options have serious negative side effects. There is growing evidence from animal studies and human clinical trials that diets rich in anthocyanins, which are pigments in fruits and vegetables, protect against inflammation and increased gut permeability as well as improve colon health through their ability to alter bacterial metabolism and the microbial milieu within the intestines. In this review, the structure and bioactivity of anthocyanins, the role of inflammation and gut bacterial dysbiosis in UC pathogenesis, and their regulation by the dietary anthocyanins are discussed, which suggests the feasibility of dietary strategies for UC mitigation.

Keywords: anthocyanins; anti-inflammatory; colitis; colonic inflammation.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The basic structure of anthocyanin.
Figure 2
Figure 2
Structures of six major anthocyanidins.
Figure 3
Figure 3
The mechanisms through which anthocyanins act as anti-inflammatory agents. Inflammatory signaling pathways including NF-kB, MAPKs (P38, ERK, JNK), and STATs were activated by ligand binding of the pro-inflammatory cytokines TNF-α, LPS, IL, and IFN, which eventually leads to the translocation of transcription factors to the nucleus, transcriptional activation, and cytokine production. Anthocyanins attenuated the cascade of inflammatory responses by inhibiting the translocation of transcription factors (P50 and P65), the phosphorylation of IRAK1, NIK, IKK, STAT1, STAT3, P38, ERK, and JNK, the secretion of inflammatory cytokines (IL-6, IL-1β, TNF-α, iNOS, COX-2, and IFN-γ), and activation of NF-kB, MAPK, and STAT inflammatory signaling pathways.

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