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Metformin inhibits pro‐inflammatory responses via targeting nuclear factor‐κB in HaCaT cells
Author(s) -
Ba Wei,
Xu Yuanyuan,
Yin Guang,
Yang Jingrun,
Wang Rui,
Chi Sumin,
Wang Yinyin,
Li Chengxin
Publication year - 2019
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.3367
Subject(s) - metformin , hacat , tumor necrosis factor alpha , inflammation , psoriasis , nf κb , nfkb1 , western blot , interleukin 6 , pharmacology , medicine , cancer research , cell culture , transcription factor , immunology , biology , endocrinology , diabetes mellitus , biochemistry , gene , genetics
Psoriasis is a prevalent, chronic inflammatory skin disease that arises from rapid and excessive growth of keratinocytes induced by abnormal inflammatory responses. Metformin is the first‐line drug in type 2 diabetes and has been proven to possess significant anti‐inflammatory effects in various diseases. In the present study, we examined the role of metformin in nuclear factor kappa B (NF‐κB)–mediated inflammatory responses in HaCaT cells, a cell line for the keratinocyte. Our results demonstrated that metformin significantly decreased the mRNA and protein levels of tumour necrosis factor‐α (TNFα), interleukin (IL)‐6, IL‐8, and IL‐1β induced by TNFα. Immunofluorescence staining and western blot analysis showed that metformin inhibited the nuclear localization of p65, a subunit of nuclear factor NF‐κB. In addition, metformin suppressed the transcription activity of NF‐κB by inhibiting the degradation of IκBα. The inhibitory effect of metformin on NF‐κB signalling is comparable with a specific IKKβ inhibitor BI605906. Collectively, our data suggest that metformin may be a potential therapeutic agent in inflammatory skin diseases like psoriasis.