Kosano H, Kayanuma T, Nishigori H
Faculty of Pharmaceutical Sciences, Teikyo University, 1091-1 Suarashi, Sagamiko-machi, Tsukui-gun, 199-0195, Kanagawa, Japan.
Biochim Biophys Acta. 2000 Dec 11;1499(1-2):11-18. doi: 10.1016/s0167-4889(00)00081-1.
The effects of 2-mercapto-1-(beta-4-pyridethyl) benzimidazole (MPB), one of the benzimidazole derivatives designed for a nucleic acid analogue, on melanogenesis of murine B16-F10 melanoma cell lines were investigated. MPB (40 microM) induced a striking dendricity in B16 melanoma cells within 12 h and maximal dendricity between 48 and 72 h. The stimulation of melanin synthesis was observed after only 2 days of treatment together with a dose-dependent growth inhibition. Moreover, MPB increased the activity of tyrosinase through the expression of tyrosinase mRNA without increasing the intracellular cyclic AMP content. MPB-induced melanogenesis was inhibited by novel protein kinase A inhibitors, KT-5720 and H-85. These findings indicate that MPB stimulated B16 cells to terminally differentiate and may be a useful drug in studying the regulation of melanogenesis.
2-巯基-1-（β-4-吡啶乙基）苯并咪唑（MPB）是一种设计用于核酸类似物的苯并咪唑衍生物，研究了其对小鼠B16-F10黑色素瘤细胞系黑色素生成的影响。MPB（40微摩尔）在12小时内诱导B16黑色素细胞出现显著的树突化，并在48至72小时达到最大树突化。仅在处理2天后就观察到黑色素合成的刺激以及剂量依赖性的生长抑制。此外，MPB通过酪氨酸酶mRNA的表达增加了酪氨酸酶的活性，而没有增加细胞内环状AMP的含量。新型蛋白激酶A抑制剂KT-5720和H-85可抑制MPB诱导的黑色素生成。这些发现表明，MPB刺激B16细胞终末分化，可能是研究黑色素生成调节的有用药物。
