Glucosamine Inhibits Lipopolysaccharide-induced Inflammatory Responses in Human Periodontal Ligament Fibroblasts
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초록
Glucosamine is commonly taken by the elderly withoutprescription as a nutritional supplement to attenuate theprogression or symptoms of osteoarthritis. Previous studiesdemonstrated that glucosamine shows anti-inflammatoryeffects in tissues such as blood vessels and the heart. However,there have been few reports about the effects of glucosamineon oral inflammatory diseases. Therefore, in this study, theeffects of glucosamine on lipopolysaccharide (LPS)-inducedinflammatory responses were investigated using humanperiodontal ligament fibroblasts (HPDLFs). HPDLFs wereincubated in the presence and absence of glucosamine (10mM) for 24 h, followed by treatment with E. coli LPS (100ng/ml) or vehicle. Quantitative RT-PCR and ELISA resultsshowed that LPS exposure significantly increased the levels ofIL-6 and IL-8 mRNA and protein, while the effect wassignificantly suppressed by glucosamine treatment. Glucosamine did not attenuate, but slightly increased, theLPS-induced activation of mitogen activated kinases (ERK,p38, JNK). However, it suppressed the LPS-induced increasein the DNA binding affinity and transcriptional activity of NF-κB. These results suggest that glucosamine exertsanti-inflammatory effects on HPDLFs exposed to LPS viainhibition of NF-κB activity, necessitating further studiesusing animal periodontitis models.
Abstract
Glucosamine is commonly taken by the elderly withoutprescription as a nutritional supplement to attenuate theprogression or symptoms of osteoarthritis. Previous studiesdemonstrated that glucosamine shows anti-inflammatoryeffects in tissues such as blood vessels and the heart. However,there have been few reports about the effects of glucosamineon oral inflammatory diseases. Therefore, in this study, theeffects of glucosamine on lipopolysaccharide (LPS)-inducedinflammatory responses were investigated using humanperiodontal ligament fibroblasts (HPDLFs). HPDLFs wereincubated in the presence and absence of glucosamine (10mM) for 24 h, followed by treatment with E. coli LPS (100ng/ml) or vehicle. Quantitative RT-PCR and ELISA resultsshowed that LPS exposure significantly increased the levels ofIL-6 and IL-8 mRNA and protein, while the effect wassignificantly suppressed by glucosamine treatment. Glucosamine did not attenuate, but slightly increased, theLPS-induced activation of mitogen activated kinases (ERK,p38, JNK). However, it suppressed the LPS-induced increasein the DNA binding affinity and transcriptional activity of NF-κB. These results suggest that glucosamine exertsanti-inflammatory effects on HPDLFs exposed to LPS viainhibition of NF-κB activity, necessitating further studiesusing animal periodontitis models.
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