title: Curcumin relieves TPA-induced Th1 inflammation in K14-VEGF transgenic mice.
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.
authors: Department of Pharmacy, General Hospital of Jinan Military Command, Jinan 250031, China.
authors: Jun
authors: J
authors: Sun
authors: Department of Pharmacy, General Hospital of Lanzhou Military Command, Lanzhou 730050, China.
authors: Yi
authors: Y
authors: Zhao
authors: Department of Pharmacy, Changhai Hospital, The Second Military Medical University, Shanghai 200433, China.
authors: Hairong
authors: H
authors: Jin
authors: Department of Pharmacy, Changhai Hospital, The Second Military Medical University, Shanghai 200433, China. Electronic address: 434772224@qq.com.
authors: Jinhong
authors: J
authors: Hu
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D003474:Curcumin / Q000494:pharmacology / Q000627:therapeutic use*; D016207:Cytokines / Q000235:genetics; D004195:Disease Models, Animal; D005782:Gels; D007249:Inflammation / Q000139:chemically induced / Q000188:drug therapy / Q000276:immunology / Q000473:pathology; D008822:Mice, Transgenic; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000276:immunology; D011565:Psoriasis / Q000139:chemically induced / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000276:immunology; D054399:Receptors, CCR6 / Q000276:immunology; D012867:Skin / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D013755:Tetradecanoylphorbol Acetate; D018417:Th1 Cells / Q000276:immunology
chemical_list: D000893:Anti-Inflammatory Agents; C498126:CCR6 protein, mouse; D016207:Cytokines; D005782:Gels; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D012333:RNA, Messenger; D016692:Receptors, Antigen, T-Cell, gamma-delta; D054399:Receptors, CCR6; C539901:Rorc protein, mouse; D003474:Curcumin; D013755:Tetradecanoylphorbol Acetate
keywords: Curcumin; Inflammation; Mouse; TPA; Transgenic