Zaidi Kamal U, Khan Firoz N, Ali Sharique A, Khan Kausar P
Biotechnology Pharmacology Laboratory, Centre for Scientific Research and Development, People's University and Saifia Science College, Bhaopal-462001, India.
Protein Pept Lett. 2019;26(12):910-918. doi: 10.2174/0929866526666190506114604.
Melanin plays a crucial role in camouflage, social communication and protection against harmful ultraviolet radiations. Melanin is synthesized by melanocytes through melanogenesis and several intrinsic and extrinsic factors are involved during the process. Any change occuring in the normal melanogenesis process can cause severe pigmentation problems of hypopigmentation or hyperpigmentation.
The present study is based on the evaluation of the effect of thymoquinone on melanogenesis and their possible mechanism of action using the B16F10 melanoma cell line for the production via blocking signaling pathways.
Phase contrast microscopy, cell viability, tyrosinase activity, melanin content and western blot analysis were used in the present study.
In the present investigation, cultured melanocytes exhibit that the stimulation of melanin synthesis when treated with thymoquinone. Tyrosinase activity and melanin production in B16F10 melanoma cell line was increased in doze-dependent manner. In western blot, we investigated the involvement of the cAMP/PKA pathway in thymoquinone induced melanogenesis. It was observed protein kinase inhibitors PKA, PKC, PKB and MEK1 decreased the stimulatory effects of thymoquinone from 11.45- fold value to 8.312, 6.631, 4.51, and 7.211-fold value, respectively. However, the results also prove that thymoquinone may partially induce tyrosinase expression via PKA, PKB, PKC and MEK1 signaling pathways.
The present finding proposed that thymoquinone is a protective challenger for melanogenesis and it might be useful for the treatment of hypopigmentary disorders.
黑色素在伪装、社交交流以及抵御有害紫外线辐射方面发挥着关键作用。黑色素由黑素细胞通过黑色素生成过程合成,该过程涉及多种内在和外在因素。正常黑色素生成过程中发生的任何变化都可能导致严重的色素沉着问题,如色素减退或色素沉着过度。
本研究基于对百里醌对黑色素生成的影响及其可能的作用机制进行评估,使用B16F10黑色素瘤细胞系通过阻断信号通路来进行研究。
本研究采用相差显微镜、细胞活力、酪氨酸酶活性、黑色素含量及蛋白质印迹分析。
在本研究中,培养的黑素细胞显示,用百里醌处理时会刺激黑色素合成。B16F10黑色素瘤细胞系中的酪氨酸酶活性和黑色素生成以剂量依赖性方式增加。在蛋白质印迹分析中,我们研究了cAMP/PKA信号通路在百里醌诱导的黑色素生成中的作用。观察到蛋白激酶抑制剂PKA、PKC、PKB和MEK1分别将百里醌的刺激作用从11.45倍值降低到8.312、6.631、4.51和7.211倍值。然而,结果也证明百里醌可能通过PKA、PKB、PKC和MEK1信号通路部分诱导酪氨酸酶表达。
本研究结果表明,百里醌是黑色素生成的一种保护性挑战因素,可能对色素减退性疾病的治疗有用。