English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Zeolite 4A, synthetic silicate, has been shown to exhibit diverse biological activities such as anti-cancer and anti-oxidant activity. In the present study, we report that the zeolite 4A may improve skin-whitening. We found that zeolite 4A inhibited melanin production in a dose-dependent manner, which has not cytotoxicity. Zeolite 4A also inhibited alpha-melanocyte-stimulating hormone (alpha-MSH)-induced melanin synthesis in B16F10 cells. Interestingly, zeolite 4A decreased alpha-MSH-induced tyrosinase activity in B16F10 cells, which did not inhibit tyrosinase activity under cell-free conditions. The results of this study indicate that zeolite 4A may reduce pigmentation by way of an indirect nonenzymatic mechanism. We also found that zeolite 4A decreased alpha-MSH-induced microphthalmia-associated transcription factor (MITF) and tyrosinase expression and that zeolite 4A induced the activation of extracellular signal-regulated kinase (ERK). These results suggest that the depigmenting effect of zeolite 4A may result from the down-regulation of MITF and tyrosinase expression by increasing ERK activity. The results thus provide evidence that zeolite 4A can be used as a potential skin-whitening agent.

biological and pharmaceutical bulletin

Zeolite 4A, a Synthetic Silicate, Suppresses Melanogenesis through the Degradation of Microphthalmia-Associated Transcription Factor by Extracellular Signal-Regulated Kinase Activation in B16F10 Melanoma Cells