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Int Immunopharmacol. 2015 Apr;25(2):235-41. doi: 10.1016/j.intimp.2015.02.007. Epub 2015 Feb 12.

Curcumin relieves TPA-induced Th1 inflammation in K14-VEGF transgenic mice.

Author information

1
Department of Pharmacy, General Hospital of Jinan Military Command, Jinan 250031, China.
2
Department of Pharmacy, General Hospital of Lanzhou Military Command, Lanzhou 730050, China.
3
Department of Pharmacy, Changhai Hospital, The Second Military Medical University, Shanghai 200433, China.
4
Department of Pharmacy, Changhai Hospital, The Second Military Medical University, Shanghai 200433, China. Electronic address: 434772224@qq.com.

Abstract

Curcumin has been confirmed to have anti-inflammatory properties in addition to the ability to decrease the expression of pro-inflammatory cytokines in keratinocytes. It was suggested that the interleukin-23 (IL-23)/IL-17A cytokine axis played a critical role in the pathogenesis of 12-O-tetradecanoyl phorbol 12-myristate 13-acetate (TPA)-induced K14-VEGF transgenic psoriasis-like mice model. Here, we report that topical use of a curcumin gel formulation inhibited TPA-induced Th1 inflammation in K14-VEGF transgenic mice ears but not Th17 inflammation as expected. Real-time PCR showed that mRNA levels of IL-23, IL-17A, IL-22, IL-6 and TNFα cytokines failed to increase after TPA-induction in K14-VEGF transgenic mice ear skin; but the mRNA level of IFNγ increased significantly at the same time. Furthermore, TPA-induction up-regulated the TCRγδ protein but failed to impact the CCR6 protein, which means that the proliferation of γδ T cells is incapable of IL-17A production. We find that curcumin is capable of relieving TPA-induced inflammation by directly down-regulating IFNγ production. In conclusion, curcumin inhibits TPA-induced Th1 inflammation in K14-VEGF transgenic mice which has not been previously described.

KEYWORDS:

Curcumin; Inflammation; Mouse; TPA; Transgenic

PMID:
25682767
DOI:
10.1016/j.intimp.2015.02.007
[Indexed for MEDLINE]

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