title: [Gallic acid inhibits inflammatory response of RAW264.7 macrophages by blocking the activation of TLR4/NF-κB induced by LPS].
abstract: Objective To observe the influence of gallic acid on Toll-like receptor 4/nuclear factor-κB (TLR4/NF-κB) pathway in the RAW264.7 macrophages stimulated by lipopolysaccharide (LPS). Methods RAW264.7 macrophages were divided into the following groups: control group, LPS group, LPS combined with gallic acid group, LPS combined with pyrrolidine dithiocarbamate (PDTC) group and LPS combined with dexamethasone (DM) group. RAW264.7 cells were cultured for 24 hours after corresponding treatments. The levels of tumor necrosis factor α (TNF-α), interleukin-1 (IL-1) and IL-6 were detected by ELISA. The levels of TLR4 and NF-κB mRNAs were tested by real-time PCR. The levels of p-IκBα, p65, p-p65 and TLR4 proteins were examined by Western blotting. Results The expression levels of TNF-α, IL-1 and IL-6 were up-regulated in the RAW264.7 macrophages after stimulated by LPS. Gallic acid could reduce the elevated expression levels of TNF-α, IL-1 and IL-6 induced by LPS. The expression of TLR4 significantly increased after stimulated by LPS and NF-κB was activated. Gallic acid could reverse the above changes and prevent the activation of NF-κB. Conclusion Gallic acid could inhibit LPS-induced inflammatory response in RAW264.7 macrophages via TLR4/NF-κB pathway.
authors.affiliation: School of Public Health, Baotou Medical College, Baotou 014060, China.
authors.forename: Lihua
authors.initials: L
authors.lastname: Huang
authors.affiliation: School of Public Health, Baotou Medical College, Baotou 014060, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Hou
authors.affiliation: School of Public Health, Baotou Medical College, Baotou 014060, China.
authors.forename: Hainan
authors.initials: H
authors.lastname: Xue
authors.affiliation: College of Veterinarian, Inner Mongolia Agricultural University, Huhhot 014010, China. *Corresponding author, E-mail: chunjiewang200@sohu.com.
authors.forename: Chunjie
authors.initials: C
authors.lastname: Wang
mesh_terms: D000818:Animals; D003907:Dexamethasone / Q000378:metabolism; D005707:Gallic Acid / Q000494:pharmacology*; D007375:Interleukin-1 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism*; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism*; D011392:Proline / Q000031:analogs & derivatives / Q000494:pharmacology; D000067996:RAW 264.7 Cells; D015398:Signal Transduction / Q000187:drug effects; D013859:Thiocarbamates / Q000494:pharmacology; D051197:Toll-Like Receptor 4 / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D007375:Interleukin-1; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; D013859:Thiocarbamates; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; C066229:prolinedithiocarbamate; D005707:Gallic Acid; D003907:Dexamethasone; D011392:Proline