RESUMO
In this study, we examined physiological functions as a key material to develop cosmeceuticals using extracts of Lagerstroemia macrocarpa Wall. Ex Kurz (L. macrocarpa). Initially, the L. macrocarpa extract was treated by different concentration and antioxidant assay (DPPH and ABTS) were performed to measure free radical scavenging ability. In the cytotoxicity experiment, the extract was treated into human epidermal keratinocytes with different concentrations to measure cytotoxicity. We found that the extract induces differentiation markers such as keratin (KRT)1, KRT2, KRT9, KRT10 in keratinocytes. Furthermore, the extract significantly induces involucrin (IVL), loricrin (LOR), claudin1 (CLDN1), and filaggrin (FLG) expression, suggesting that it may enhance skin barrier functions. Especially, the extract restored FLG expression inhibited by interleukin (IL)-4/IL-13 in in vitro atopic dermatitis-like model. Therefore, we expect L. macrocarpa extract will be an effective material to develop the therapeutic and cosmeceutical of atopic dermatitis.
Assuntos
Dermatite Atópica , Lagerstroemia , Humanos , Lagerstroemia/metabolismo , Dermatite Atópica/tratamento farmacológico , Dermatite Atópica/metabolismo , Proteínas de Filamentos Intermediários/metabolismo , Proteínas de Filamentos Intermediários/farmacologia , Proteínas de Filamentos Intermediários/uso terapêutico , Estrutura Molecular , Queratinócitos , Extratos Vegetais/metabolismo , Transdução de Sinais , Fator de Transcrição STAT6/metabolismo , Fator de Transcrição STAT6/farmacologiaRESUMO
Human blinding disorders are often initiated by hereditary mutations that insult rod and/or cone photoreceptors and cause subsequent cellular death. Generally, the disease phenotype can be predicted from the specific mutation as many photoreceptor genes are specific to rods or cones; however certain genes, such as Retinal Degeneration Slow (RDS), are expressed in both cell types and cause different forms of retinal disease affecting rods, cones, or both photoreceptors. RDS is a transmembrane glycoprotein critical for photoreceptor outer segment disc morphogenesis, structural maintenance, and renewal. Studies using animal models with Rds mutations provide valuable insight into Rds gene function and regulation; and a better understanding of the physiology, pathology, and underlying degenerative mechanisms of inherited retinal disease. Furthermore, these models are an excellent tool in the process of developing therapeutic interventions for the treatment of inherited retinal degenerations. In this paper, we review these topics with particular focus on the use of rds models in gene therapy.