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Inhibition of Ca2+-permeable TRPV3 and inflammatory cytokine release by honokiol and magnolol in human epidermal keratinocytes.
- Source :
-
Biochemical & Biophysical Research Communications . Jan2024, Vol. 692, pN.PAG-N.PAG. 1p. - Publication Year :
- 2024
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Abstract
- Transient receptor potential vanilloid-3 (TRPV3) ion channels are prominently expressed in keratinocytes, playing a vital role in skin functions. Honokiol and magnolol (H&M) the primary bioactive constituents in Magnolia officinalis extract, demonstrate anti-inflammatory and skin-protective properties. Nevertheless, the underlying mechanism regarding their effect on Ca2+-permeable ion channels remain unclear. Our purpose in this study is to investigate the effect of H&M on TRPV3 and cytokine release in normal human epidermal keratinocytes (NHEKs), including its gain-of-function (GOF) mutants (G573S and G573C) associated with Olmstead syndrome. We performed whole-cell patch-clamp, fura-2 spectrofluorimetry to investigate channels activity, CCK-8 assay to analyze cell death and enzyme-linked immunosorbent assay to assess the cytokine release from NHEKs. H&M inhibited the TRPV3 current (I TRPV3) and cytosolic calcium increase in NHEKs, HEK293T cells overexpressing hTRPV3 and its GOF mutants. Moreover, the release of pro-inflammatory cytokines (interleukin-6 and -8) from keratinocytes stimulated by TRPV3 agonist was effectively suppressed by H&M. Our findings provide insights into the mechanism underlying the anti-inflammatory effects of H&M, highlighting their potential in treating skin diseases. [Display omitted] • Honokiol and magnolol (H&M) inhibit TRPV3 in human epidermal keratinocytes. • H&M inhibit overactive TRPV3 variants linked with Olmsted syndrome. • H&M suppress IL-6 and IL-8 release through TRPV3 in keratinocytes. • H&M can be potentially used to treat inflammatory skin diseases. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 0006291X
- Volume :
- 692
- Database :
- Academic Search Index
- Journal :
- Biochemical & Biophysical Research Communications
- Publication Type :
- Academic Journal
- Accession number :
- 174560402
- Full Text :
- https://doi.org/10.1016/j.bbrc.2023.149332