Finanda Anwar Harfina, Seok Park Chang, Manggau Marianti, Yun Hye-Young, Kim Dong-Seok
Department of Biochemistry, Chung-Ang University College of Medicine, Seoul 06974, Republic of Korea.
Faculty of Pharmacy, Hasanuddin University, Makassar 90245, Indonesia.
J Tradit Chin Med. 2025 Jun;45(3):485-492. doi: 10.19852/j.cnki.jtcm.2025.03.005.
In the present study, we investigated the effects of jatropholone B from () on melanin synthesis in Mel-Ab cells.
Mel-Ab cells were cultured to measure melanin content and tyrosinase activities. Western blotting was performed to investigate jatropholone B-induced signal transduction and measure the expression of melanogenic proteins.
Jatropholone B decreased melanin synthesis in a concentration-dependent manner but did not directly inhibit the activity of tyrosinase, a melanogenic enzyme. Instead, jatropholone B downregulated microphthalmia-associated transcription factor (MITF) and tyrosinase protein levels. Therefore, we investigated jatropholone B-induced signal transduction related to MITF and tyrosinase expression. However, jatropholone B had no significant effect on Akt and glycogen synthase kinase-3β phosphorylation as well as β-catenin change. In contrast, jatropholone B was observed to phosphorylate extracellular signal-regulated kinase (ERK) for the first time. To clarify the involvement of ERK activation in jatropholone B-induced hypopigmentation, we pretreated cells with PD98059, a specific ERK pathway inhibitor, and measured MITF and tyrosinase levels as well as melanin content. PD98059 pretreatment abrogated jatropholone B-induced downregulation of MITF and tyrosinase expression as well as reduction in melanin production.
Based on these results, we suggest that ERK activation by jatropholone B inhibits melanogenesis the downregulation of MITF and tyrosinase expression. Therefore, jatropholone B from J. curcas can be a candidate for developing a new skin-whitening agent.
在本研究中,我们研究了来自[具体来源未给出]的麻风树醇酮B对Mel-Ab细胞中黑色素合成的影响。
培养Mel-Ab细胞以测量黑色素含量和酪氨酸酶活性。进行蛋白质免疫印迹法以研究麻风树醇酮B诱导的信号转导并测量黑色素生成相关蛋白的表达。
麻风树醇酮B以浓度依赖性方式降低黑色素合成,但不直接抑制黑色素生成酶酪氨酸酶的活性。相反,麻风树醇酮B下调小眼相关转录因子(MITF)和酪氨酸酶蛋白水平。因此,我们研究了与MITF和酪氨酸酶表达相关的麻风树醇酮B诱导的信号转导。然而,麻风树醇酮B对Akt和糖原合酶激酶-3β磷酸化以及β-连环蛋白变化没有显著影响。相比之下,首次观察到麻风树醇酮B使细胞外信号调节激酶(ERK)磷酸化。为了阐明ERK激活在麻风树醇酮B诱导的色素减退中的作用,我们用特异性ERK途径抑制剂PD98059预处理细胞,并测量MITF和酪氨酸酶水平以及黑色素含量。PD98059预处理消除了麻风树醇酮B诱导的MITF和酪氨酸酶表达下调以及黑色素生成减少。
基于这些结果,我们认为麻风树醇酮B激活ERK通过下调MITF和酪氨酸酶表达来抑制黑色素生成。因此,来自麻风树的麻风树醇酮B可以作为开发新型皮肤美白剂的候选物。