摘要
目的研究丹皮酚抑制黑素合成的相关的信号转导途径。方法以B16F10黑素瘤细胞系为对象,用不同的有丝分裂原活化蛋白激酶(MAPK)信号途径干预物和丹皮酚共同处理细胞,采用多巴氧化法测定酪氨酸酶活性,氢氧化钠裂解法检测黑素含量,RT-PCR和Western blot检测酪氨酸酶的mRNA以及蛋白表达;并以Western blot法检测丹皮酚对不同MAPK途径关键激酶磷酸化蛋白表达的调节作用。结果在不同的MAPK信号途径抑制剂中,JNK1/2/3特异性抑制剂(SP600125)能够有效地拮抗丹皮酚对黑素合成的抑制作用,而且丹皮酚能够诱导磷酸化JNK/SAPK表达。结论JNK/SAPK途径参与了介导丹皮酚对黑素合成的抑制作用。
Aim To investigate mitogen-activated protein kinase signaling pathways （MAPKs） paeonol-induced inhibition of melanogenesis. mediating Methods B16F10 melanoma cells treated with paeonol and va- rious inhibitors of MAPK signaling pathways. Melanin content and tyrosinase activity were measured by dopa oxidase assay and NaOH-assay respectively, mRNA and protein expression of tyrosinase were detected by RT-PCR and Western blot respectively. Protein levels of phosphorylated MAPKs in B16F10 cells treated with paeonol were examined by western blot analysis. Resuits Among various MAPK inhibitors, a selective inhibitor of JNK1/2/3 （ SP600125 ） significantly reversed down-regulation of melanogenesis response to paeonol （200 μmol·L^-l） , and Western blot analysis showed that paeonol （200 μmol·L^-l ） obviously in-duced phosphorylation of JNK/SAPK. Conclusions JNK/SAPK signal transduction pathway may be involved in the mediation of the inhibition of melanogene- sis induced by paeonol.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2008年第7期915-919,共5页
Chinese Pharmacological Bulletin
基金
江苏省自然科学基金资助项目(NoBK2003016)
