Lamin A-dependent nuclear aberration and DNA damage was found in premature aging disease or normally old individuals. In this study, UVB irradiation was used as a cellular senescence inducer, and it was found that Lamin A and phospho-H2AX protein was increased by UVB treatment on normal human fibroblast. Lamin A-dependent morphological nuclear defect was observed in UVB treated fibroblast. Amentoflavone, a well known biflavonoid, inhibited the increase of Lamin A or phospho-H2AX protein in dose dependent manner which was induced by UVB irradiation, and also protected nuclear aberration dramatically. These results indicated that amentoflavone is an anti-aging candidate for UVB related skin aging process.
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