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首页> 外文期刊>Biochemical Pharmacology >The anti-melanogenic effects of ellagic acid through induction of autophagy in melanocytes and suppression of UVA-activated ?-MSH pathways via Nrf2 activation in keratinocytes
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The anti-melanogenic effects of ellagic acid through induction of autophagy in melanocytes and suppression of UVA-activated ?-MSH pathways via Nrf2 activation in keratinocytes

机译：鞣果诱导鞣酸抗搅拌效应通过在角蛋白酶细胞中通过NRF2活化诱导脲瘤中的自噬和抑制UVA活化的α-MSH途径

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摘要

Ellagic acid (EA) is a natural phenol antioxidant in different fruits, vegetables, and nuts. As a copper iron chelator from the tyrosinase enzyme?s active site, EA was reported to inhibit melanogenesis in melanocytes. Here, we demonstrated the anti-melanogenic mechanisms of EA through autophagy induction in melanoma B16F10 cells and the role of Nrf2 and UVA (3 J/cm2)-activated ?-melanocyte stimulating hormone (?-MSH) pathways in keratinocyte HaCaT cells. In vitro data showed that EA suppressed the tyrosinase activity and melanogenesis by suppressing cAMP-mediated CREB and MITF signaling mechanisms in ?-MSH-stimulated B16F10 cells. ERK, JNK, and AKT pathways were involved in this EA-regulated MITF downregulation. Notably, EA induced autophagy in B16F10 cells was evidenced from increased LC3-II accumulation, p62/SQSTM1 activation, ATG4B downregulation, acidic vesicular organelle (AVO) formation, PI3K/AKT/mTOR inhibition, and Beclin-1/Bcl-2 dysregulation. Interestingly, 3-MA (an autophagy inhibitor) pretreatment or LC3 silencing (siRNA transfection) of B16F10 cells significantly reduced EA-induced anti-melanogenic activity. Besides this, in UVAirradiated keratinocyte HaCaT cells, EA suppressed ROS production and ?-MSH generation. Moreover, EA mediated the activation and nuclear translocation of Nrf2, leading to antioxidant ?-GCLC, HO-1, and NQO-1 protein expression in HaCaT cells. However, Nrf2 knockdown has significantly impaired this effect, and there was an uncontrolled ROS generation following UVA irradiation. JNK, PKC, and ROS pathways were involved in the activation of Nrf2 in HaCaT cells. In vivo experiments using the zebrafish model confirmed that EA inhibited tyrosinase activity and endogenous pigmentation. In conclusion, ellagic acid is an effective skin-whitening agent and might be used as a topical applicant.
机译：鞣花酸（EA）是不同水果，蔬菜和坚果的天然酚抗氧化剂。作为来自酪氨酸酶酶的铜螯合剂的铜螯合剂，据报道EA抑制黑素细胞中的黑素瘤。在这里，我们通过黑色素瘤B16F10细胞中的自噬诱导和NRF2和UVA（3J / cm2）的作用证明了EA的抗批发机制，以及在角蛋白细胞HACAT细胞中的NRF2和UVA（3J / cm2） - 术刺激的β-melanocyte刺激激素（β-msh）途径。体外数据显示EA通过抑制脉冲介导的CREB和MITF信号传导机制抑制酪氨酸酶活性和黑素生成的α-MMSH刺激的B16F10细胞。 ERK，JNK和AKT途径参与了这个EA监管的MITF下调。值得注意的是，AE诱导B16F10细胞中的自噬来自LC3-II积累，P62 / SQSTM1活化，ATG4b下调，酸性囊细胞器（AVO）形成，PI3K / AKT / mTOR抑制，和BECLIN-1 / BCL-2的诱导剂。有趣的是，B16F10细胞的3- mA（自噬抑制剂）预处理或LC3沉默（siRNA转染）显着降低了EA诱导的抗丝杀菌活性。除此之外，在uvairradiated角蛋白细胞hacat细胞中，EA抑制了ROS生产和？-MSH生成。此外，EA介导NRF2的活化和核转位，导致抗氧化剂α-GCLC，HO-1和HACAT细胞中的NQO-1蛋白表达。然而，NRF2敲低度显着受损了这种效果，并且在UVA辐照后存在不受控制的ROS生成。 JNK，PKC和ROS途径参与了HACAT细胞中NRF2的激活。使用斑马鱼模型的体内实验证实EA抑制酪氨酸酶活性和内源性色素沉着。总之，鞣花酸是一种有效的皮肤增白剂，可用作局部申请人。

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