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首页> 外文期刊>Experimental dermatology >Partially purified Curcuma longa inhibits alpha-melanocyte-stimulating hormone-stimulated melanogenesis through extracellular signal-regulated kinase or Akt activation-mediated signalling in B16F10 cells.
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Partially purified Curcuma longa inhibits alpha-melanocyte-stimulating hormone-stimulated melanogenesis through extracellular signal-regulated kinase or Akt activation-mediated signalling in B16F10 cells.

机译:部分纯化的姜黄通过B16F10细胞中的细胞外信号调节激酶或Akt激活介导的信号传导抑制α-黑素细胞刺激激素刺激的黑色素生成。

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摘要

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.
机译:通过溶剂分配进行生物测定指导的姜黄分级分离,并用十八烷基硅烷开放柱色谱纯化,得到部分纯化。来自乙酸乙酯层的活性80%甲醇色谱馏分(从长条梭菌(PPC)进行部分纯化)用于研究B16F10细胞中由α-黑素细胞刺激激素(alpha-MSH)刺激的黑素生成信号途径。在刺激α-MSH的细胞中,PPC抑制细胞黑色素含量,酪氨酸酶活性和黑色素生成相关蛋白(包括小眼症相关转录因子(MITF),酪氨酸酶和酪氨酸酶相关蛋白(TRP))的表达。 PPC在α-MSH刺激的B16F10细胞中激活了黑色素生成调节信号,如促分裂原活化蛋白激酶(MEK)/细胞外信号调节激酶(ERK)和磷脂酰肌醇3-激酶(PI3K)/ Akt。通过选择性抑制MEK / ERK(PD98059)和PI3K(LY294002),废除了PPC对α-MSH诱导的黑色素生成的抑制活性。 PPC激活的MEK / ERK或Akt可能通过MITF及其下游信号途径(包括酪氨酸酶和TRP)在α-MSH诱导的黑色素生成中通过黑色素合成减少。

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