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Gallic Acid-g-Chitosan Modulates Inflammatory Responses in LPS-Stimulated RAW264.7 Cells Via NF-κB, AP-1, and MAPK Pathways.
Inflammation. 2016 Feb; 39(1):366-374.I

Abstract

Chitosan is a naturally occurring polysaccharide, which has exhibited antioxidant, antimicrobial, and anti-cancer activities among others. Modification of chitosan by grafting phenolic compounds is a good strategy for improvement of bioactivities of chitosan. We investigated the anti-inflammatory action of gallic acid-grafted-chitosan (GAC) in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. GAC inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2) by inhibiting inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in LPS-stimulated RAW264.7 macrophages. GAC also suppressed the production and mRNA expression of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). GAC inactivated nuclear factor-κB (NF-κB) via inhibiting the phosphorylation and degradation of the NF-κB inhibitor, IκB. In addition, GAC suppresses the activation of activator protein-1 (AP-1) through the phosphorylation of mitogen-activated protein kinase (MAPK) such as extracellular signal-regulated kinase (ERK1/2), p38 MAPK, and c-Jun N-terminal kinase/stress-activated protein kinase (JNK). These results suggest that GAC has the potential anti-inflammatory action by downregulating transcriptional factors (NF-κB and AP-1) through MAPK signaling pathways.

Authors+Show Affiliations

Division of Food and Nutrition, Chonnam National University, Gwangju, 550-757, Republic of Korea.Department of Biomedical Engineering, Pukyong National University, Busan, 608-737, Republic of Korea.Department of Chemistry, Pukyong National University, Busan, 608-737, Republic of Korea.Department of Food Science and Biotechnology, Kunsan National University, Kunsan, 573-701, Republic of Korea.Major in Pharmaceutical Engineering, Division of Bioindustry, Silla University, Busan, 46958, Republic of Korea.Department of Marine-Bio Convergence Science, Pukyong National University, Busan, 608-739, Republic of Korea. jjy1915@pknu.ac.kr.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26412258

Citation

Ahn, Chang-Bum, et al. "Gallic Acid-g-Chitosan Modulates Inflammatory Responses in LPS-Stimulated RAW264.7 Cells Via NF-κB, AP-1, and MAPK Pathways." Inflammation, vol. 39, no. 1, 2016, pp. 366-374.
Ahn CB, Jung WK, Park SJ, et al. Gallic Acid-g-Chitosan Modulates Inflammatory Responses in LPS-Stimulated RAW264.7 Cells Via NF-κB, AP-1, and MAPK Pathways. Inflammation. 2016;39(1):366-374.
Ahn, C. B., Jung, W. K., Park, S. J., Kim, Y. T., Kim, W. S., & Je, J. Y. (2016). Gallic Acid-g-Chitosan Modulates Inflammatory Responses in LPS-Stimulated RAW264.7 Cells Via NF-κB, AP-1, and MAPK Pathways. Inflammation, 39(1), 366-374. https://doi.org/10.1007/s10753-015-0258-2
Ahn CB, et al. Gallic Acid-g-Chitosan Modulates Inflammatory Responses in LPS-Stimulated RAW264.7 Cells Via NF-κB, AP-1, and MAPK Pathways. Inflammation. 2016;39(1):366-374. PubMed PMID: 26412258.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Gallic Acid-g-Chitosan Modulates Inflammatory Responses in LPS-Stimulated RAW264.7 Cells Via NF-κB, AP-1, and MAPK Pathways. AU - Ahn,Chang-Bum, AU - Jung,Won-Kyo, AU - Park,Sun-Joo, AU - Kim,Yong-Tae, AU - Kim,Won-Suk, AU - Je,Jae-Young, PY - 2015/9/29/entrez PY - 2015/9/29/pubmed PY - 2016/12/15/medline KW - AP-1 KW - MAPK KW - NF-κB KW - RAW macrophage KW - chitosan KW - inflammation SP - 366 EP - 374 JF - Inflammation JO - Inflammation VL - 39 IS - 1 N2 - Chitosan is a naturally occurring polysaccharide, which has exhibited antioxidant, antimicrobial, and anti-cancer activities among others. Modification of chitosan by grafting phenolic compounds is a good strategy for improvement of bioactivities of chitosan. We investigated the anti-inflammatory action of gallic acid-grafted-chitosan (GAC) in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. GAC inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2) by inhibiting inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in LPS-stimulated RAW264.7 macrophages. GAC also suppressed the production and mRNA expression of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). GAC inactivated nuclear factor-κB (NF-κB) via inhibiting the phosphorylation and degradation of the NF-κB inhibitor, IκB. In addition, GAC suppresses the activation of activator protein-1 (AP-1) through the phosphorylation of mitogen-activated protein kinase (MAPK) such as extracellular signal-regulated kinase (ERK1/2), p38 MAPK, and c-Jun N-terminal kinase/stress-activated protein kinase (JNK). These results suggest that GAC has the potential anti-inflammatory action by downregulating transcriptional factors (NF-κB and AP-1) through MAPK signaling pathways. SN - 1573-2576 UR - https://www.unboundmedicine.com/medline/citation/26412258/Gallic_Acid_g_Chitosan_Modulates_Inflammatory_Responses_in_LPS_Stimulated_RAW264_7_Cells_Via_NF_κB_AP_1_and_MAPK_Pathways_ L2 - https://doi.org/10.1007/s10753-015-0258-2 DB - PRIME DP - Unbound Medicine ER -