Sato Kazuomi, Toriyama Masaru
Department of Applied Biological Chemistry, Faculty of Agriculture, Shizuoka University, 836 Ohya, Shizuoka, 422-8529, Japan.
J Dermatol Sci. 2009 Feb;53(2):140-5. doi: 10.1016/j.jdermsci.2008.08.017. Epub 2008 Nov 17.
Increased production and accumulation of melanin leads to various hyperpigmentation disorders. Melanin synthesis is regulated by melanogenic proteins such as tyrosinase, tyrosinase-related protein (TRP)-1 and -2, and their transcription factors.
In this study, we assessed the effects of PQQ on melanogenic protein expression of murine B16 melanoma cells.
We assessed melanin production of PQQ-treated B16 melanoma cells. Furthermore, we investigated the effect of PQQ on the activity of melanogenic enzymes and their expression using Western blot and semi-quantitative RT-PCR analyses.
In the present study, PQQ inhibited melanin synthesis in cultured melanoma cells stimulated by either alpha-melanocyte stimulating hormone (alpha-MSH) or 3-isobutyl-1-methylxanthine (IBMX). To elucidate the mechanism of the effect of PQQ on melanogenesis, we performed Western blotting for melanogenic proteins, such as tyrosinase, TRP-1, and TRP-2. PQQ inhibited tyrosinase expression, however, it did not inhibit TRP-2 expression. Used as the stimulant for melanogenesis, both alpha-MSH and IBMX gave the same results for melanogenic protein expression. Semi-quantitative RT-PCR analysis showed that the depigmentation effect of PQQ might be due to the inhibition of tyrosinase gene transcription but not the inhibition of microphthalmia-associated transcription factor (Mitf).
This report indicates that PQQ is a possible anti-melanogenic agent and might be effective against hyperpigmentation disorders.
黑色素生成增加和积累会导致各种色素沉着过度紊乱。黑色素合成受黑素生成蛋白如酪氨酸酶、酪氨酸酶相关蛋白(TRP)-1和-2及其转录因子调控。
在本研究中,我们评估了吡咯喹啉醌(PQQ)对小鼠B16黑色素瘤细胞黑素生成蛋白表达的影响。
我们评估了经PQQ处理的B16黑色素瘤细胞的黑色素生成。此外,我们使用蛋白质免疫印迹法和半定量逆转录-聚合酶链反应(RT-PCR)分析研究了PQQ对黑素生成酶活性及其表达的影响。
在本研究中,PQQ抑制了由α-黑素细胞刺激素(α-MSH)或3-异丁基-1-甲基黄嘌呤(IBMX)刺激的培养黑色素瘤细胞中的黑色素合成。为阐明PQQ对黑色素生成影响的机制,我们对黑素生成蛋白如酪氨酸酶、TRP-1和TRP-2进行了蛋白质免疫印迹分析。PQQ抑制了酪氨酸酶表达,然而,它并未抑制TRP-2表达。作为黑色素生成的刺激物,α-MSH和IBMX对黑素生成蛋白表达产生了相同的结果。半定量RT-PCR分析表明,PQQ的色素脱失作用可能是由于抑制了酪氨酸酶基因转录而非小眼相关转录因子(Mitf)的抑制。
本报告表明PQQ可能是一种抗黑素生成剂,可能对色素沉着过度紊乱有效。