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Tea catechins reduce inflammatory reactions via mitogen-activated protein kinase pathways in toll-like receptor 2 ligand-stimulated dental pulp cells.

Abstract

AIMS

In this study, we evaluated whether catechins could inhibit the expression of pro-inflammatory mediators induced by dental caries-related bacteria, Streptococci, or pathogen-associated molecular patterns (PAMPs) stimulation in human dental pulp fibroblasts (HDPF). We further determined the mechanisms of the anti-inflammatory activity of catechins.

MAIN METHODS

Streptococci or PAMP-stimulated HDPF were treated with catechin, and then the expression and production of pro-inflammatory mediators were determined by RT-PCR and ELISA. Furthermore, the signal transduction pathways activated with toll-like receptor (TLR)2 ligand were assessed by Immunoblot and ELISA using blocking assay with specific inhibitors.

KEY FINDINGS

Increased expressions of pro-inflammatory mediators are found in inflamed dental pulp, especially in HDPF. We recently reported that dental pulpal innate immune responses may mainly result from the predominantly-expressed TLR2 signaling. Catechins, polyphenolic compounds in green tea, exert protective and healing effects through multiple mechanisms, including antioxidative and anti-inflammatory effects. However, there are no reports concerning the effects of catechins on dental pulp. In this study, we demonstrated that the up-regulated expressions of IL-8 or PGE(2) in Streptococci or PAMP-stimulated HDPF were inhibited by catechins, (-)-epicatechin gallate (ECG) and (-)-epigallocatechin gallate (EGCG). In TLR2 ligand-stimulated HDPF, specific inhibitors of extracellular signal regulated kinase (ERK)1/2, p38, c-jun NH(2)-terminal kinase (SAP/JNK), NF-kappaB or catechins markedly reduced the level of pro-inflammatory mediators and the phosphorylation of these signal transduction molecules was suppressed by catechins.

SIGNIFICANCE

These findings suggest that catechins might be useful therapeutically as an anti-inflammatory modulator of dental pulpal inflammation.

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  • Publisher Full Text
  • Authors+Show Affiliations

    ,

    Department of Conservative Dentistry, Institute of Health Biosciences, The University of Tokushima Graduate School, Japan.

    , , , , ,

    Source

    Life sciences 86:17-18 2010 Apr 24 pg 654-60

    MeSH

    Anti-Inflammatory Agents
    Catechin
    Cells, Cultured
    Dental Pulp
    Enzyme-Linked Immunosorbent Assay
    Fibroblasts
    Humans
    Inflammation
    Inflammation Mediators
    Ligands
    Mitogen-Activated Protein Kinases
    Phosphorylation
    Receptors, Pattern Recognition
    Reverse Transcriptase Polymerase Chain Reaction
    Signal Transduction
    Streptococcus
    Tea
    Toll-Like Receptor 2
    Up-Regulation

    Pub Type(s)

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

    Language

    eng

    PubMed ID

    20176036

    Citation

    Hirao, Kouji, et al. "Tea Catechins Reduce Inflammatory Reactions Via Mitogen-activated Protein Kinase Pathways in Toll-like Receptor 2 Ligand-stimulated Dental Pulp Cells." Life Sciences, vol. 86, no. 17-18, 2010, pp. 654-60.
    Hirao K, Yumoto H, Nakanishi T, et al. Tea catechins reduce inflammatory reactions via mitogen-activated protein kinase pathways in toll-like receptor 2 ligand-stimulated dental pulp cells. Life Sci. 2010;86(17-18):654-60.
    Hirao, K., Yumoto, H., Nakanishi, T., Mukai, K., Takahashi, K., Takegawa, D., & Matsuo, T. (2010). Tea catechins reduce inflammatory reactions via mitogen-activated protein kinase pathways in toll-like receptor 2 ligand-stimulated dental pulp cells. Life Sciences, 86(17-18), pp. 654-60. doi:10.1016/j.lfs.2010.02.017.
    Hirao K, et al. Tea Catechins Reduce Inflammatory Reactions Via Mitogen-activated Protein Kinase Pathways in Toll-like Receptor 2 Ligand-stimulated Dental Pulp Cells. Life Sci. 2010 Apr 24;86(17-18):654-60. PubMed PMID: 20176036.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Tea catechins reduce inflammatory reactions via mitogen-activated protein kinase pathways in toll-like receptor 2 ligand-stimulated dental pulp cells. AU - Hirao,Kouji, AU - Yumoto,Hiromichi, AU - Nakanishi,Tadashi, AU - Mukai,Kayo, AU - Takahashi,Kanako, AU - Takegawa,Daisuke, AU - Matsuo,Takashi, Y1 - 2010/02/20/ PY - 2009/11/04/received PY - 2010/02/11/revised PY - 2010/02/12/accepted PY - 2010/2/24/entrez PY - 2010/2/24/pubmed PY - 2010/4/22/medline SP - 654 EP - 60 JF - Life sciences JO - Life Sci. VL - 86 IS - 17-18 N2 - AIMS: In this study, we evaluated whether catechins could inhibit the expression of pro-inflammatory mediators induced by dental caries-related bacteria, Streptococci, or pathogen-associated molecular patterns (PAMPs) stimulation in human dental pulp fibroblasts (HDPF). We further determined the mechanisms of the anti-inflammatory activity of catechins. MAIN METHODS: Streptococci or PAMP-stimulated HDPF were treated with catechin, and then the expression and production of pro-inflammatory mediators were determined by RT-PCR and ELISA. Furthermore, the signal transduction pathways activated with toll-like receptor (TLR)2 ligand were assessed by Immunoblot and ELISA using blocking assay with specific inhibitors. KEY FINDINGS: Increased expressions of pro-inflammatory mediators are found in inflamed dental pulp, especially in HDPF. We recently reported that dental pulpal innate immune responses may mainly result from the predominantly-expressed TLR2 signaling. Catechins, polyphenolic compounds in green tea, exert protective and healing effects through multiple mechanisms, including antioxidative and anti-inflammatory effects. However, there are no reports concerning the effects of catechins on dental pulp. In this study, we demonstrated that the up-regulated expressions of IL-8 or PGE(2) in Streptococci or PAMP-stimulated HDPF were inhibited by catechins, (-)-epicatechin gallate (ECG) and (-)-epigallocatechin gallate (EGCG). In TLR2 ligand-stimulated HDPF, specific inhibitors of extracellular signal regulated kinase (ERK)1/2, p38, c-jun NH(2)-terminal kinase (SAP/JNK), NF-kappaB or catechins markedly reduced the level of pro-inflammatory mediators and the phosphorylation of these signal transduction molecules was suppressed by catechins. SIGNIFICANCE: These findings suggest that catechins might be useful therapeutically as an anti-inflammatory modulator of dental pulpal inflammation. SN - 1879-0631 UR - https://www.unboundmedicine.com/medline/citation/20176036/Tea_catechins_reduce_inflammatory_reactions_via_mitogen_activated_protein_kinase_pathways_in_toll_like_receptor_2_ligand_stimulated_dental_pulp_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(10)00078-0 DB - PRIME DP - Unbound Medicine ER -