UNLABELLED: Ethyl alcohol (ethanol) is commonly applied in cosmetic and pharmaceutical preparations, as well as disinfectant for chronic wounds. OBJECTIVE: The present study aimed to appraise physiological levels of ethanol-induced damage in skin cells in vitro and the possible repair by hyaluronic acid (HA). In addition, we aimed to establish cytokine-chemokine networks in the cellular media and the modulation of cytokines such as tumor necrosis factor-alpha (TNF-B), interferon-alpha (IFN-α), transforming growth factor-beta (TGF-B), interleukins (IL) such as IL1-B and IL-6, as well as matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP). DESIGN AND METHODS: We treated human A431 epidermoid skin cells and mouse fibroblasts with ethanol at a concentration of 100 mM over 24 hours (h). A separate experiment looked at the effects of 2 consecutive treatments with 100 mM ethanol for 24 h each. HA obtained from umbilical cord excision was used at two concentration levels (2% and 4%) to determine its efficacy in the treatment. We measured cytotoxicity and cytokine networks in the media. RESULTS: Treatment of cells with 100 mM ethanol increased cytotoxicity, as well as the release of pro-inflammatory cytokines into the culture medium. CONCLUSIONS: Ethanol may induce cytotoxicity in skin cells by enhancing the effects of pro-inflammatory cytokines. HA reduced the amount of pro-inflammatory cytokines released into the media both in human A431 epidermoid skin cells and in mouse fibroblasts.
UNLABELLED: Ethyl alcohol (ethanol) is commonly applied in cosmetic and pharmaceutical preparations, as well as disinfectant for chronic wounds. OBJECTIVE: The present study aimed to appraise physiological levels of ethanol-induced damage in skin cells in vitro and the possible repair by hyaluronic acid (HA). In addition, we aimed to establish cytokine-chemokine networks in the cellular media and the modulation of cytokines such as tumor necrosis factor-alpha (TNF-B), interferon-alpha (IFN-α), transforming growth factor-beta (TGF-B), interleukins (IL) such as IL1-B and IL-6, as well as matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP). DESIGN AND METHODS: We treated human A431 epidermoid skin cells and mouse fibroblasts with ethanol at a concentration of 100 mM over 24 hours (h). A separate experiment looked at the effects of 2 consecutive treatments with 100 mM ethanol for 24 h each. HA obtained from umbilical cord excision was used at two concentration levels (2% and 4%) to determine its efficacy in the treatment. We measured cytotoxicity and cytokine networks in the media. RESULTS: Treatment of cells with 100 mM ethanol increased cytotoxicity, as well as the release of pro-inflammatory cytokines into the culture medium. CONCLUSIONS:Ethanol may induce cytotoxicity in skin cells by enhancing the effects of pro-inflammatory cytokines. HA reduced the amount of pro-inflammatory cytokines released into the media both in human A431 epidermoid skin cells and in mouse fibroblasts.
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