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首页> 外文期刊>Journal of dermatological science >Kojic acid-induced IL-6 production in human keratinocytes plays a role in its anti-melanogenic activity in skin
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Kojic acid-induced IL-6 production in human keratinocytes plays a role in its anti-melanogenic activity in skin

机译：曲酸诱导人角质形成细胞中IL-6的产生在皮肤中具有抗黑色素生成的作用

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Background: Kojic acid is a fungal metabolite widely used in medicinal and cosmetic formulations as a skin-lightening agent based on its de-pigmenting activity. Although in human clinical studies kojic acid has been shown to be effective in the treatment of hyper-pigmentation disorders such as melasma, the reasons for its apparent lack of anti-melanogenic activity in cultured mammalian melanocytes are unclear. Objectives: This study was aimed to elucidate pharmacological mechanisms of the in vivo anti-melanogenic activity of kojic acid in human skin. Methods: A primary human melanocyte and keratinocyte co-culture system was used to evaluate whether kojic-acid-induced changes in keratinocytes were associated with anti-melanogenic activities in melanocytes. The cytokine secretion profiles in response to kojic acid were analyzed. Results: Kojic acid increased interleukin (IL)-6 and IL-8 production in melanocyte/keratinocyte co-cultures; however, IL-6 directly inhibited melanogenesis whereas IL-8 did not. In melanocyte monocultures, kojic acid did not increase IL-6 production whereas in keratinocyte monocultures it significantly up-regulated IL-6 gene and protein expression. Therefore, the up-regulation of IL-6 in melanocyte/keratinocyte co-cultures seems to be originated from kojic acid-induced changes in keratinocytes. Anti-IL-6 antibody treatment antagonized the anti-melanogenic effect of kojic acid on the co-cultures. Conclusions: The pharmacological mechanism of kojic acid to explain clinically effective anti-melanogenic activity on hyper-pigmented skin is associated with the kojic acid-induced IL-6 production in keratinocytes. The cross-talk between melanocytes and keratinocytes should be determined in future studies on the pharmacological mechanisms of clinically effective dermatological drugs acting on the epidermis.
机译：背景：曲酸是一种真菌代谢产物，由于其具有脱色活性，因此广泛用作药物和化妆品制剂中的亮肤剂。尽管在人类临床研究中已显示曲酸可有效治疗色素沉着过度的疾病，例如黑斑病，但在培养的哺乳动物黑素细胞中明显缺乏抗黑素活性的原因尚不清楚。目的：本研究旨在阐明人体内曲酸的体内抗黑色素生成活性的药理机制。方法：使用原代人黑素细胞和角质形成细胞共培养系统评估曲酸诱导的角质形成细胞变化是否与黑素细胞的抗黑素形成活性相关。分析了响应曲酸的细胞因子分泌概况。结果：曲酸增加了黑素细胞/角质形成细胞共培养物中白介素（IL）-6和IL-8的产生;但是，IL-6直接抑制黑色素生成，而IL-8没有。在黑素细胞单培养中，曲酸不会增加IL-6的产生，而在角质形成细胞单培养中，曲酸会明显上调IL-6基因和蛋白质的表达。因此，黑素细胞/角质形成细胞共培养物中IL-6的上调似乎源于曲酸诱导的角质形成细胞变化。抗IL-6抗体处理拮抗曲酸对共培养物的抗黑色素生成作用。结论：曲酸的药理机制可解释对色素沉着过度的皮肤具有有效的抗黑色素生成活性，这与曲酸诱导的角质形成细胞中IL-6的产生有关。黑色素细胞和角质形成细胞之间的串扰应在将来的研究中，对作用于表皮的临床有效皮肤病学药物的药理机制进行研究。

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