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Chinese Journal of Stomatology ; (12): 737-741, 2014.
Article in Chinese | WPRIM | ID: wpr-360488

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the influence of high glucose on Porphyromonasgingivalis (Pg) lipopolysaccharide (LPS) stimulating human gingival fibroblasts (HGF) to secret the cytokines.</p><p><b>METHODS</b>HGF were obtained from the primary culture of the tissue explants. Cells were divided into four groups, low glucose (5.5 mmol/L) + 1 mg/L Pg LPS (group A);low glucose + 10 mg/L Pg LPS (group B); high glucose (25 mmol/L) +1 mg/L Pg LPS(group C); high glucose+10 mg/L Pg LPS (group D). The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in cell supernatants were detected by enzyme- linked immunosorbent assay at 6 h and 12 h. The expressions of toll-like receptor 2, 4 (TLR-2, 4) were examined by real-time polymerase chain reaction. After pretreatment with anti-TLR2 and anti-TLR4 monoclonal antibody in HGF, TNF-α and L-1β levels were detected.</p><p><b>RESULTS</b>TNF-α concentration increased obviously in high glucose 6 h and 12 h after Pg LPS stimulation (P < 0.01). IL-1β secretion increased (P < 0.01). Meanwhile, TLR2, 4 mRNA expression increased, especially in high glucose+10 mg/L Pg LPS (P < 0.01). After inhibition of the TLR2, 4 in high glucose + 10 mg/L Pg LPS respectively, TNF-α level [(297.16±11.49), (390.01±12.81) ng/L] decreased (F = 166.02, P < 0.01), and IL-1β level [(49.90±4.08), (99.35±5.01) ng/L] also decreased (F = 153.51, P < 0.01).</p><p><b>CONCLUSIONS</b>High glucose may promote Pg LPS to stimulate the secretion of TNF-α and IL-1β through regulating TLR2, 4 expression, which suggests that the elevating blood glucose precipitate in aggravating the process of periodontal disease.</p>


Subject(s)
Humans , Antibodies, Monoclonal , Drug Synergism , Fibroblasts , Metabolism , Glucose , Pharmacology , Interleukin-1beta , Metabolism , Periodontal Diseases , Polysaccharides, Bacterial , Toxicity , Porphyromonas gingivalis , Chemistry , Time Factors , Toll-Like Receptor 2 , Allergy and Immunology , Metabolism , Toll-Like Receptor 4 , Allergy and Immunology , Metabolism , Tumor Necrosis Factor-alpha , Metabolism
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