title: Capsaicin regulates the NF-κB pathway in salivary gland inflammation.
abstract: Salivary gland epithelial cells (SGEC) release several cytokines that play important roles in the inflammatory process. In this study, we examined whether capsaicin can modulate cytokine release in SGEC. After cells were stimulated with polyinosinic-polycytidylic acid [poly(I:C)] or lipopolysaccharide (LPS), mRNA transcript and protein levels were detected by reverse-transcriptase-polymerase chain-reaction (RT-PCR), real-time PCR, and enzyme-linked immunosorbent assay (ELISA). These findings demonstrated that the increases in TNFα and IL-6 mRNA transcripts were highest at 3 hrs and 1 hr after incubation with poly(I:C) and LPS, respectively. Pre-treatment of the cells with 10 μµ capsaicin, however, significantly inhibited mRNA transcripts and its protein levels. The simultaneous application of 10 μµ capsazepine with capsaicin did not block the inhibitory effect of capsaicin. Furthermore, the inhibitory effect of capsaicin was also shown in primary cultured cells from TRPV1(-/-) mice. We found that both poly(I:C) and LPS induced IκB-α degradation and phosphorylation, which resulted in NF-κB activation, and capsaicin inhibited this NF-κB pathway. These results demonstrate that SGEC release pro-inflammatory cytokines mediated by TLR, and capsaicin inhibits this process through the NF-κB pathway. This study suggests that capsaicin could potentially alleviate inflammation in salivary glands.
authors.affiliation: Department of Physiology, School of Dentistry, Seoul National University and Dental Research Institute, Seoul 110-749, Korea.
authors.forename: Y-H
authors.initials: YH
authors.lastname: Shin
authors.forename: E
authors.initials: E
authors.lastname: Namkoong
authors.forename: S
authors.initials: S
authors.lastname: Choi
authors.forename: J-S
authors.initials: JS
authors.lastname: Bae
authors.forename: M
authors.initials: M
authors.lastname: Jin
authors.forename: S-M
authors.initials: SM
authors.lastname: Hwang
authors.forename: R
authors.initials: R
authors.lastname: Arote
authors.forename: S-Y
authors.initials: SY
authors.lastname: Choi
authors.forename: K
authors.initials: K
authors.lastname: Park
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002211:Capsaicin / Q000031:analogs & derivatives / Q000494:pharmacology*; D002478:Cells, Cultured; D016207:Cytokines / Q000187:drug effects; D004847:Epithelial Cells / Q000187:drug effects; D004926:Escherichia coli; D020672:I-kappa B Proteins / Q000187:drug effects; D018836:Inflammation Mediators / Q000494:pharmacology; D015850:Interleukin-6 / Q000032:analysis; D008070:Lipopolysaccharides / Q000494:pharmacology; D051379:Mice; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000187:drug effects*; D010766:Phosphorylation; D011070:Poly I-C / Q000494:pharmacology; D018987:Salivary Ducts / Q000166:cytology / Q000187:drug effects; D012793:Sialadenitis / Q000276:immunology*; D013363:Submandibular Gland / Q000166:cytology / Q000187:drug effects; D050916:TRPV Cation Channels / Q000187:drug effects; D013997:Time Factors; D051193:Toll-Like Receptors / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D020672:I-kappa B Proteins; D018836:Inflammation Mediators; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; C000606205:Nfkbia protein, mouse; D050916:TRPV Cation Channels; C493921:TRPV1 protein, mouse; D051193:Toll-Like Receptors; D014409:Tumor Necrosis Factor-alpha; D000072000:NF-KappaB Inhibitor alpha; C071423:capsazepine; D011070:Poly I-C; D002211:Capsaicin
keywords: IL-6; TNF-alpha; TRPV1 receptor; anti-inflammatory; capsazepine; toll-like receptor