Toll-like receptor 4/nuclear factor-κB signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect

Xinying Yang; Guojian Zhang; Xuelian Tang; Jieying Jiao; Sung Yeon Kim; Joo Young Lee; Tianjiao Zhu; Dehai Li; Yong Gab Yun; Qianqun Gu; Hyun Park

doi:10.1007/s11010-012-1502-9

Toll-like receptor 4/nuclear factor-κB signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect

Xinying Yang
, Guojian Zhang
, Xuelian Tang
, Jieying Jiao
, Sung Yeon Kim
, Joo Young Lee
, Tianjiao Zhu
, Dehai Li
, Yong Gab Yun
, Qianqun Gu
, Hyun Park

Wonkwang University
CAS - Shanghai Institute of Materia Medica
Ocean University of China
South China Agricultural University

Research output: Contribution to journal › Article › peer-review

10 Scopus citations

Abstract

ACTG-toxin H (AH) originates from Alternaria sp. In this study, we explored the molecular mechanism underlying the anti-inflammatory properties of AH. Treatment with AH inhibited lipopolysaccharide (LPS)-induced interleukin-6, IL-1β, inducible nitric oxide synthase, and cyclooxygenase-2 expression and nitric oxide production. Furthermore, AH inhibited LPS-induced P38 MAPK and Akt activation in RAW264.7 cells. Electrophoretic mobility shift assays (EMSAs) showed that AH inhibited LPS-induced nuclear factor-κB (NFκB) DNA-binding activity. Using transfection assay and measurement of an NFκB-sensitive promoter region, we found that transfection of toll-like receptor 4 (TLR4) increased LPS-induced NFκB transcription activity in 293T cells. AH significantly blocked LPS-induced NFκB activation in TLR4-transfected cells. Taken together, our data indicated that anti-inflammatory properties of AH resulted from the inhibition of proinflammatory cytokines and enzyme production via the TLR4/NFκB signaling pathway.

Original language	English
Pages (from-to)	29-36
Number of pages	8
Journal	Molecular and Cellular Biochemistry
Volume	374
Issue number	1-2
DOIs	https://doi.org/10.1007/s11010-012-1502-9
State	Published - Feb 2013

Bibliographical note

Funding Information:
Acknowledgments The research was supported by the Public Welfare & Safety Research Program through the National Research Foundation (NRF) funded by the Ministry of Education, Science and Technology (20120006545); the Chinese National Natural Science Fund (30973627); and a grant from Shandong Province of China (No. ZR2009CZ016).

Keywords

ACTG-toxin H
LPS
TLR4/NFκB

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10.1007/s11010-012-1502-9

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title = "Toll-like receptor 4/nuclear factor-κB signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect",

abstract = "ACTG-toxin H (AH) originates from Alternaria sp. In this study, we explored the molecular mechanism underlying the anti-inflammatory properties of AH. Treatment with AH inhibited lipopolysaccharide (LPS)-induced interleukin-6, IL-1β, inducible nitric oxide synthase, and cyclooxygenase-2 expression and nitric oxide production. Furthermore, AH inhibited LPS-induced P38 MAPK and Akt activation in RAW264.7 cells. Electrophoretic mobility shift assays (EMSAs) showed that AH inhibited LPS-induced nuclear factor-κB (NFκB) DNA-binding activity. Using transfection assay and measurement of an NFκB-sensitive promoter region, we found that transfection of toll-like receptor 4 (TLR4) increased LPS-induced NFκB transcription activity in 293T cells. AH significantly blocked LPS-induced NFκB activation in TLR4-transfected cells. Taken together, our data indicated that anti-inflammatory properties of AH resulted from the inhibition of proinflammatory cytokines and enzyme production via the TLR4/NFκB signaling pathway.",

keywords = "ACTG-toxin H, LPS, TLR4/NFκB",

author = "Xinying Yang and Guojian Zhang and Xuelian Tang and Jieying Jiao and Kim, \{Sung Yeon\} and Lee, \{Joo Young\} and Tianjiao Zhu and Dehai Li and Yun, \{Yong Gab\} and Qianqun Gu and Hyun Park",

note = "Funding Information: Acknowledgments The research was supported by the Public Welfare \& Safety Research Program through the National Research Foundation (NRF) funded by the Ministry of Education, Science and Technology (20120006545); the Chinese National Natural Science Fund (30973627); and a grant from Shandong Province of China (No. ZR2009CZ016).",

year = "2013",

month = feb,

doi = "10.1007/s11010-012-1502-9",

language = "English",

volume = "374",

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journal = "Molecular and Cellular Biochemistry",

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T1 - Toll-like receptor 4/nuclear factor-κB signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect

AU - Yang, Xinying

AU - Zhang, Guojian

AU - Tang, Xuelian

AU - Jiao, Jieying

AU - Kim, Sung Yeon

AU - Lee, Joo Young

AU - Zhu, Tianjiao

AU - Li, Dehai

AU - Yun, Yong Gab

AU - Gu, Qianqun

AU - Park, Hyun

N1 - Funding Information: Acknowledgments The research was supported by the Public Welfare & Safety Research Program through the National Research Foundation (NRF) funded by the Ministry of Education, Science and Technology (20120006545); the Chinese National Natural Science Fund (30973627); and a grant from Shandong Province of China (No. ZR2009CZ016).

PY - 2013/2

Y1 - 2013/2

N2 - ACTG-toxin H (AH) originates from Alternaria sp. In this study, we explored the molecular mechanism underlying the anti-inflammatory properties of AH. Treatment with AH inhibited lipopolysaccharide (LPS)-induced interleukin-6, IL-1β, inducible nitric oxide synthase, and cyclooxygenase-2 expression and nitric oxide production. Furthermore, AH inhibited LPS-induced P38 MAPK and Akt activation in RAW264.7 cells. Electrophoretic mobility shift assays (EMSAs) showed that AH inhibited LPS-induced nuclear factor-κB (NFκB) DNA-binding activity. Using transfection assay and measurement of an NFκB-sensitive promoter region, we found that transfection of toll-like receptor 4 (TLR4) increased LPS-induced NFκB transcription activity in 293T cells. AH significantly blocked LPS-induced NFκB activation in TLR4-transfected cells. Taken together, our data indicated that anti-inflammatory properties of AH resulted from the inhibition of proinflammatory cytokines and enzyme production via the TLR4/NFκB signaling pathway.

AB - ACTG-toxin H (AH) originates from Alternaria sp. In this study, we explored the molecular mechanism underlying the anti-inflammatory properties of AH. Treatment with AH inhibited lipopolysaccharide (LPS)-induced interleukin-6, IL-1β, inducible nitric oxide synthase, and cyclooxygenase-2 expression and nitric oxide production. Furthermore, AH inhibited LPS-induced P38 MAPK and Akt activation in RAW264.7 cells. Electrophoretic mobility shift assays (EMSAs) showed that AH inhibited LPS-induced nuclear factor-κB (NFκB) DNA-binding activity. Using transfection assay and measurement of an NFκB-sensitive promoter region, we found that transfection of toll-like receptor 4 (TLR4) increased LPS-induced NFκB transcription activity in 293T cells. AH significantly blocked LPS-induced NFκB activation in TLR4-transfected cells. Taken together, our data indicated that anti-inflammatory properties of AH resulted from the inhibition of proinflammatory cytokines and enzyme production via the TLR4/NFκB signaling pathway.

KW - ACTG-toxin H

KW - LPS

KW - TLR4/NFκB

UR - https://www.scopus.com/pages/publications/84871960757

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DO - 10.1007/s11010-012-1502-9

M3 - Article

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AN - SCOPUS:84871960757

SN - 0300-8177

VL - 374

SP - 29

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JO - Molecular and Cellular Biochemistry

JF - Molecular and Cellular Biochemistry

IS - 1-2

ER -

Toll-like receptor 4/nuclear factor-κB signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect

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