Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 19, Pages -Publisher
MDPI
DOI: 10.3390/ijms221910326
Keywords
claudin; keratinocyte; UVB; nitric oxide; apigenin; flavonoid
Funding
- JSPS KAKENHI [19H03373]
- Hoyu Science Foundation
- Cosmetology Foundation
- Ogawa Science and Technology Foundation
- Yamada Bee Company, Inc.
- Grants-in-Aid for Scientific Research [19H03373] Funding Source: KAKEN
Ask authors/readers for more resources
The study demonstrated that Brazilian green propolis ethanol extract and flavonoids have a protective effect against weak UVB-induced skin barrier dysfunction, in particular apigenin and apigenin-like flavonoids, by suppressing NO production and CLDN1 mislocalization. The chemically and structurally characteristic flavonoids with a hydroxyl group at the 4 ' position on the B-ring were found to contribute to their protective effect on barrier dysfunction caused by weak UVB irradiation.
Once weak ultraviolet ray-B (UVB) irradiates the skin cells, the generation of reactive nitrogen species (RNS), but not reactive oxygen species (ROS), is stimulated for the mislocalization of claudin-1 (CLDN1), an essential protein for forming tight junctions (TJs). Since our skin is constantly exposed to sunlight throughout our lives, an effective protection strategy is needed to maintain the skin barrier against weak UVB. In the present study, we investigated whether an ethanol extract of Brazilian green propolis (EBGP) and flavonoids had a protective effect against weak UVB irradiation-induced barrier dysfunction in human keratinocyte-derived HaCaT cells. A pretreatment with EBGP suppressed TJ permeability, RNS production, and the nitration level of CLDN1 in the weak UVB-exposed cells. Among the propolis components, apigenin and apigenin-like flavonoids have potent protective effects against NO production and the mislocalization of CLDN1 induced by UVB. The analyses between structures and biological function revealed that the chemically and structurally characteristic flavonoids with a hydroxyl group at the 4 ' position on the B-ring might contribute to its protective effect on barrier dysfunction caused by weak UVB irradiation. In conclusion, EBGP and its component apigenin protect HaCaT cells from weak UVB irradiation-induced TJ barrier dysfunction mediated by suppressing NO production.
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