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Journal of Korean Academy of Conservative Dentistry ; : 153-160, 2006.
Article in English | WPRIM | ID: wpr-174010

ABSTRACT

We investigated the secretion of Interleukin-8 (IL-8) from ginviva and periodontal ligament stimulated with Substance P (SP) and Calcitonin Gene-related Peptide (CGRP). Gingiva (GF), periodontal ligament (PDLF) and pulp (PF) tissues were collected from extracted intact 3rd molars. Cultured cells were stimulated with different concentrations of SP for 4 hrs, and stimulated with SP, CGRP and Tumor Necrosis Factor-alpha (TNF-alpha) for 8 hrs. Then RNase Protection Assay was carried out. ELISA was performed using supernatants of stimulated cells for quantitative analysis of IL-8. Results were assessed using student t-test with significance of P < 0.05. According to this study, the results were as follows: 1. IL-8 mRNA was detected in all type of cells studied (PF, GF and PDLF). 2. IL-8 mRNA expression was not increased after stimulating 4 hrs with SP (10(-5)M) and SP (10(-8)M) compared with Mock stimulation in all type of cells studied. 3. IL-8 mRNA expression was not increased after stimulating 8 hrs with SP (10(-4)M) and CGRP (10(-6)M) compared with Mock stimulation in all type of cells studied. 4. TNF-alpha(2 ng/ml) increased the expression of IL-8 mRNA in all kind of cells studied. 5. The secretion of IL-8 from GF was increased 8 hrs after the stimulation with CGRP (10(-6)M) (p < 0.05). 6. The secretion of IL-8 from PDLF was increased 8 hrs after the stimulation with SP (10(-4)M) (p < 0.05). Calcitonin Gene-related Peptide (CGRP) increased Interleukin-8 (IL-8) which plays an important role in chemotaxis of neutrophil in Calcitonin Gene-related Peptide (CGRP) gingival tissue, whereas Substance P increased the secretion of IL-8 from periodontal ligament.


Subject(s)
Humans , Calcitonin Gene-Related Peptide , Cells, Cultured , Chemotaxis , Enzyme-Linked Immunosorbent Assay , Gingiva , Interleukin-8 , Molar , Neuropeptides , Neutrophils , Periodontal Ligament , Ribonucleases , RNA, Messenger , Substance P , Tumor Necrosis Factor-alpha
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