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.

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Epigenetic alteration of the purinergic type 7 receptor in salivary epithelial cells

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“TRP inflammation” relationship in cardiovascular system

“…In salivary glands, polyinosinic-polycytidylic acid or LPS activates, via TLR4 activation, NF-κB by IκB-α degradation and phosphorylation to release highly proinflammatory cytokines TNFα and IL-6. Capsaicin inhibits this process by interacting with the NF-κB pathway whereby to potentially alleviate inflammation of salivary glands [43]. Indeed, in healthy human subjects as well as patients, capsaicin has been suggested to have a therapeutic potential alone or in combination with other non-steroidal anti-inflammatory drugs [44], and in a mouse CLP model, capsaicin is shown to relieve the damaging impact of sepsis through TRPV1 activation [44,45] MSU, cholesterol, amyloid-β, and ambient particle matter MSU A uric acid crystal, monosodium urate (MSU), has emerged as an important factor for both gouty arthritis and immune regulation.…”