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Photodermatol Photoimmunol Photomed. 2009 Oct;25(5):250-8. doi: 10.1111/j.1600-0781.2009.00454.x.

Mitigation of acute ultraviolet B radiation-mediated damages by baicalin in mouse skin.

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  • 1Department of Dermatology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.



Solar ultraviolet (UV) irradiation, in particular UVB with a wavelength range between 290 and 320 nm, induces different hazardous effects on the skin, including sunburn, photoaging and cancer. Protection against sun-induced damage is therefore a highly desirable goal. Chemoprevention is being investigated as a potential approach for the management of UV damages including skin cancer.


In this study, to determine the relevance of our in vitro findings to in vivo situations, we assessed the effects of baicalin on UVB-mediated damages in mice skin.


Balb/C hairless mice were topically pretreated (24 h before UVB) or post-treated (5 min after UVB) with baicalin (1 mg/cm(2) skin area/mouse/100 microl acetone) and were exposed to UVB 24 h later (180 mJ/cm(2)). The animals were sacrificed 1 and 24 h after the UVB exposure. Skin edema, histopathology changes, hydrogen peroxide (H2O2) and cyclobutane pyrimidine dimers (CPDs)-positive cells were assessed to determine the UVB-induced photodamage.


Our data demonstrated that a topical application of baicalin, either as a pretreatment or as a post-treatment, resulted in a significant decrease in UVB mediated increases in skin edema, skin hyperplasia and infiltration of leukocytes. Further, baicalin treatments (pre and post) also resulted in a significant decrease in UVB mediated (1) generation of H2O2 and (2) formation of DNA photolesions: CPDs.


Based on these data, we suggest that baicalin could be developed as an agent for the management of conditions elicited by UV exposure including skin cancer.

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