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Pharmacol Rep. 2017 Oct;69(5):1030-1035. doi: 10.1016/j.pharep.2017.04.006. Epub 2017 Apr 18.

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

Author information

1
Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: kimwoonhae@cu.ac.kr.
2
Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: ahj119@cu.ac.kr.
3
Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: jy1118@cu.ac.kr.
4
Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: daldy99@naver.com.
5
Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: asdf8760@naver.com.
6
Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: pathosjlee@cu.ac.kr.
7
Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: pathpjy@naver.com.
8
Department of Dermatology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: gdpk1217@naver.com.
9
Department of Agricultural Biology, National Academy of Agricultural Science, Rural Development Administration, 300, Nongsaengmyeong-ro, Wansan-gu, Jeonju-si, Jeollabuk-do 54875, Republic of Korea. Electronic address: sangmih@korea.kr.
10
Department of Pathology, College of Medicine, Dongguk University, 123, Dongdae-ro, Gyeongju-si, Gyeongsangbuk-do 38066, Republic of Korea. Electronic address: minkyungk76@naver.com.
11
Department of Pathology, College of Medicine, Catholic University of Daegu, 33, Duryugongwon-ro 17-gil, Nam-gu, Daegu 42472, Republic of Korea. Electronic address: kkpark@cu.ac.kr.

Abstract

BACKGROUND:

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.

METHODS:

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.

RESULTS:

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.

CONCLUSIONS:

These results suggest that apamin has therapeutic effect on AD through improvement of inflammatory condition.

KEYWORDS:

Apamin; Atopic dermatitis; NF-κB; STAT; Type 2 helper T lymphocyte chemokine

PMID:
28958612
DOI:
10.1016/j.pharep.2017.04.006
[Indexed for MEDLINE]

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