Apamin inhibits TNF-α- and IFN-γ-induced inflammatory cytokines and chemokines via suppressions of NF-κB signaling pathway and STAT in human keratinocytes

Atopic dermatitis (AD) is identified by an increase in infiltrations of several inflammatory cells including type 2 helper (Th2) lymphocytes. Th2-related chemokines such as thymus and activation-regulated chemokine (TARC/CCL17) and macrophage-derived chemokine (MDC/CCL22), and pro-inflammatory cytok...

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Bibliographic Details
Published in:Pharmacological reports 2017-10, Vol.69 (5), p.1030-1035
Main Authors: Kim, Woon-Hae, An, Hyun-Jin, Kim, Jung-Yeon, Gwon, Mi-Gyeong, Gu, Hyemin, Lee, Sun-Jae, Park, Ji Y., Park, Kyung-Duck, Han, Sang-Mi, Kim, Min-Kyung, Park, Kwan-Kyu
Format: Article
Language:English
Subjects:
Apamin
Apamin - pharmacology
Atopic dermatitis
Cell Line
Cell Survival - drug effects
Cytokines - genetics
Cytokines - metabolism
Cytokines - pharmacology
Drug Safety and Pharmacovigilance
Gene Expression Regulation - drug effects
Humans
Interferon-gamma - pharmacology
Keratinocytes - drug effects
Keratinocytes - metabolism
NF-kappa B - genetics
NF-kappa B - metabolism
NF-κB
Original Article
Pharmacotherapy
Pharmacy
STAT
STAT Transcription Factors - metabolism
Tumor Necrosis Factor-alpha - pharmacology
Type 2 helper T lymphocyte chemokine
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Summary:Atopic dermatitis (AD) is identified by an increase in infiltrations of several inflammatory cells including type 2 helper (Th2) lymphocytes. Th2-related chemokines such as thymus and activation-regulated chemokine (TARC/CCL17) and macrophage-derived chemokine (MDC/CCL22), and pro-inflammatory cytokines including interleukin (IL)-1β and IL-6 are considered to play a crucial role in AD. Tumor necrosis factor (TNF)-α- and interferon (IFN)-γ induce the inflammatory condition through production of TARC, MDC, IL-1β and IL-6, and activations of related transcription factors, such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and signal transducer and activator of transcription (STAT) in keratinocytes. Apamin, a peptide component of bee venom, has been reported its beneficial activities in various diseases. However, anti-inflammatory effects of apamin on inflammatory condition in keratinocytes have not been explored. Therefore, the present study aimed to demonstrate the anti-inflammatory effect of apamin on TNF-α- and IFN-γ-induced inflammatory condition in keratinocytes. HaCaT was used as human keratinocytes cell line. Cell Counting Kit-8 was performed to measure a cytotoxicity of apamin. The effects of apamin on TNF-α-/IFN-γ-induced inflammatory condition were determined by real-time PCR and Western blot analysis. Further, NF-κB signaling pathways, STAT1, and STAT3 were analyzed by Western blot and immunofluorescence. Apamin ameliorated the inflammatory condition through suppression of Th2-related chemokines and pro-inflammatory cytokines. Further, apamin down-regulated the activations of NF-κB signaling pathways and STATs in HaCaT cells. These results suggest that apamin has therapeutic effect on AD through improvement of inflammatory condition.
ISSN:1734-1140
2299-5684
DOI:10.1016/j.pharep.2017.04.006