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部分纯化的姜黄通过细胞外信号调节激酶或Akt激活介导的信号通路抑制α-黑素细胞刺激素刺激的B16F10细胞黑素生成。

Partially purified Curcuma longa inhibits alpha-melanocyte-stimulating hormone-stimulated melanogenesis through extracellular signal-regulated kinase or Akt activation-mediated signalling in B16F10 cells.

作者信息

Jang Ji Yeon, Lee Jun Hyuk, Jeong Seong Yun, Chung Kyung Tae, Choi Yung Hyun, Choi Byung Tae

机构信息

Division of Meridian and Structural Medicine, School of Oriental Medicine, Pusan National University, Busan 609-735, Korea.

出版信息

Exp Dermatol. 2009 Aug;18(8):689-94. doi: 10.1111/j.1600-0625.2009.00857.x. Epub 2009 Mar 7.

DOI:10.1111/j.1600-0625.2009.00857.x
PMID:19469902
Abstract

Bioassay-guided fractionation of Curcuma longa by solvent partitioning and purification with octadecylsilane open column chromatography yielded a partial purification. The active 80% methanol chromatographic fraction from the ethyl acetate layer [partial purification from C. longa (PPC)] was used to investigate the alpha-melanocyte-stimulating hormone (alpha-MSH)-stimulated melanogenesis signal pathway in B16F10 cells. In cells stimulated alpha-MSH, PPC inhibited cellular melanin contents, tyrosinase activity and expression of melanogenesis-related proteins including microphthalmia-associated transcription factor (MITF), tyrosinase and tyrosinase-related proteins (TRP). Melanogenesis-regulating signalling such as mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinase (PI3K)/Akt was activated by PPC in alpha-MSH-stimulated B16F10 cells. The suppressive activity of PPC on alpha-MSH-induced melanogenesis was abrogated by selective inhibition of MEK/ERK (PD98059) and PI3K (LY294002). MEK/ERK or Akt activation by PPC may contribute to reduced melanin synthesis via MITF and its downstream signal pathway including tyrosinase and TRPs in alpha-MSH-induced melanogenesis.

摘要

通过溶剂分配和十八烷基硅烷开放柱色谱法对姜黄进行生物测定指导的分级分离,得到了部分纯化产物。来自乙酸乙酯层的活性80%甲醇色谱级分[来自姜黄的部分纯化产物(PPC)]用于研究α-黑素细胞刺激素(α-MSH)刺激的B16F10细胞中的黑素生成信号通路。在α-MSH刺激的细胞中,PPC抑制细胞黑色素含量、酪氨酸酶活性以及包括小眼相关转录因子(MITF)、酪氨酸酶和酪氨酸酶相关蛋白(TRP)在内的黑素生成相关蛋白的表达。在α-MSH刺激的B16F10细胞中,PPC激活了丝裂原活化蛋白激酶(MEK)/细胞外信号调节激酶(ERK)和磷脂酰肌醇3激酶(PI3K)/Akt等黑素生成调节信号通路。通过选择性抑制MEK/ERK(PD98059)和PI3K(LY294002),PPC对α-MSH诱导的黑素生成的抑制活性被消除。PPC对MEK/ERK或Akt的激活可能通过MITF及其下游信号通路(包括酪氨酸酶和TRP)导致α-MSH诱导的黑素生成中黑色素合成减少。

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