Epigallocatechin-3-gallate (EGCG) inhibits imiquimod-induced psoriasis-like inflammation of BALB/c mice.

Abstract:

BACKGROUND:Psoriasis is a chronic inflammatory immune disease with undefined pathogenesis. It is associated with T cells, and the IL-23/IL17 axis is believed to be crucial in the pathogenesis. The present treatments have side effects that influence the compliance of patients. Tea polyphenol is extracted from tea polyphenols, and its main active ingredient is Epigallocatechin-3-gallate (EGCG), which has been shown to have antioxidant, anti-tumor, and anti-ultraviolet radiation effects. Here, we aim to report that EGCG can inhibit imiquimod (IMQ)-induced psoriasis-like inflammation. METHODS:We used BALB/c mice, which were topically treated with IMQ for 6 consecutive days, as a psoriasis mouse model. Topical application of EGCG and treatment with EGCG were conducted in the experiments. Then observed the effects of the two methods on psoriasis-like mice dermatitis. Statistics are presented as the means ± standard error of mean (SEM) and compared using unpaired two-tailed Student's t tests or one-way ANOVA. RESULTS:Topical application of EGCG alleviated psoriasiform dermatitis, improved the skin pathological structure by reduce the expression of epidermal PCNA, promoted the expression of caspase-14. Treatment with EGCG attenuated skin inflammation, accompanied by reduced infiltrations of T cells; reduced percentages of CD11c(+) DC in the composition of immunocytes of spleens; reduced levels of interleukin (IL)-17A, IL-17F, IL-22, IL-23 and malondialdehyde (MDA) in plasma; increased percentages of CD4(+) T cells in the composition of immunocytes of spleens; and increased bioactivities of superoxide dismutase (SOD) and catalase (CAT) in plasma. CONCLUSIONS:All the results demonstrated that EGCG had anti-inflammatory, immune regulatory and antioxidant effects. It is a promising intervention in psoriasis in the future.

authors

Zhang S,Liu X,Mei L,Wang H,Fang F

doi

10.1186/s12906-016-1325-4

subject

Has Abstract

pub_date

2016-08-31 00:00:00

pages

334

issue

1

issn

1472-6882

pii

10.1186/s12906-016-1325-4

journal_volume

16

pub_type

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