Zhong Hui, An Xiaohong, Li Yu, Cai Minxuan, Ahmad Owais, Shang Jing, Zhou Jia
School of Traditional Chinese Pharmacy, China Pharmaceutical University Nanjing 211198 P. R. China
Shanghai Key Laboratory of Crime Scene Evidence, Shanghai Research Institute of Criminal Science and Technology Zhongshan North No. 1 Road Shanghai 200083 China.
RSC Adv. 2019 Jun 14;9(33):18747-18757. doi: 10.1039/c8ra09786k.
Vitiligo is an intriguing depigmentation disorder that affects about 0.5-2% of the world population. In the past decade, first-line treatments of vitiligo have involved the use of calcineurin inhibitors and corticosteroids. Sodium tanshinone IIA sulfonate (STS) has been widely applied in the treatment of cardiovascular and cerebrovascular diseases in China. In the present study, the effect of STS on melanogenesis was confirmed in the B16F10 cells and zebrafish by direct observation. The prevention of hydrogen peroxide (HO)-induced oxidative stress has been proven to be beneficial to vitiligo patients, and STS that can protect the B16F10 cells against oxidative stress has been investigated in the present reversed study. Moreover, we found that pre-treatment with STS led to a concentration-dependent mitochondrial impairment and decreased cell apoptosis of the B16F10 cells in response to HO. In addition, we demonstrated that STS increased melanin synthesis in the B16F10 cells by activating the mitogen-activated protein kinase (MAPK) and protein kinase A (PKA) pathways. STS also increased the Cdc42 and KIF5b expression to stimulate the translocation of melanin. These results suggest that STS protects the B16F10 cells against HO-induced oxidative stress and exerts melanin synthesis activity in the B16F10 cells by activating the MAPK and PKA pathways; thus, it shows therapeutic potential for vitiligo.
白癜风是一种引人关注的色素脱失性疾病，影响着全球约0.5%-2%的人口。在过去十年中，白癜风的一线治疗方法包括使用钙调神经磷酸酶抑制剂和皮质类固醇。丹参酮IIA磺酸钠（STS）在中国已被广泛应用于心血管和脑血管疾病的治疗。在本研究中，通过直接观察证实了STS在B16F10细胞和斑马鱼中对黑色素生成的影响。已证明预防过氧化氢（HO）诱导的氧化应激对白癜风患者有益，并且在本反向研究中对能够保护B16F10细胞免受氧化应激的STS进行了研究。此外，我们发现用STS预处理会导致浓度依赖性的线粒体损伤，并减少B16F10细胞对HO的细胞凋亡。此外，我们证明STS通过激活丝裂原活化蛋白激酶（MAPK）和蛋白激酶A（PKA）途径增加B16F10细胞中的黑色素合成。STS还增加Cdc42和KIF5b的表达以刺激黑色素的转运。这些结果表明，STS保护B16F10细胞免受HO诱导的氧化应激，并通过激活MAPK和PKA途径在B16F10细胞中发挥黑色素合成活性；因此，它显示出对白癜风的治疗潜力。
