Journal
JOURNAL OF DENTAL RESEARCH
Volume 92, Issue 6, Pages 547-552Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/0022034513487376
Keywords
TNF-alpha; IL-6; capsazepine; TRPV1 receptor; toll-like receptor; anti-inflammatory
Categories
Funding
- National Research Foundation of Korea Grant, through the Oromaxillofacial Dysfunction Research Center for the Elderly at Seoul National University in Korea [2012-000912]
Ask authors/readers for more resources
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 TNF alpha 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 mu M apsaicin, however, significantly inhibited mRNA transcripts and its protein levels. The simultaneous application of 10 mu M 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 I kappa B-alpha degradation and phosphorylation, which resulted in NF-kappa B activation, and capsaicin inhibited this NF-kappa B pathway. These results demonstrate that SGEC release proinflammatory cytokines mediated by TLR, and capsaicin inhibits this process through the NF-kappa B pathway. This study suggests that capsaicin could potentially alleviate inflammation in salivary glands.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available