The p38 MAPK can activate the cAMP response element binding protein, and CREB activates MITF expression, which positively contributes to melanin produc tion. The selleck chemical results in Figure 4C provide evidence that Lycium chinense Miller root SFE could inactivate CREB, JNK and p38, in turn inhibiting MITF expression. Furthermore, Protein kinase A signal ing is also reported to be involved in melanin production. The MSH mediated elevation of cellular cAMP levels could activate PKA. In turn, activated PKA can acti vate CREB, leading to the activation of MITF transcrip tional activity and resulting in the expressions of melanogenesis related proteins. Our results shown in Figure 5 also suggest that Lycium chinense Miller root SFE inhibits melanin synthesis by blocking the PKA pathway.

The ABTS free radical has been widely applied to esti mate the free radical scavenging activity of antioxidants. Antioxidants can either transfer electrons or hydrogen atoms to ABTS, thus neutralizing the species free radical character. In the present study, the Lycium chinense Miller root SFE showed lower free radical scavenging activ ities compared to the activity of Vitamin C or BHA. When assaying the total phenolic content of the Lycium chinense Miller root SFE, it was interesting to find that a higher concentration of the root extract has a highertotal phenolic content. This is probably due to most bioactive compounds such as polyphenols including tannins and flavonoid in the extracts. Polyphenols are one of the major plant compounds with antioxidant activity.

The antioxidant activity of phenolic compounds is re ported to be mainly due to their redox properties, which can play an important role in adsorbing and neutralizing free radicals, quenching singlet and triplet oxygen or de composing peroxides. To confirm the antioxidant capacity of Lycium chinense Miller root SFE in a cellular environment, intracellular ROS levels were evaluated. The principle of the assay is based on the fact that DCFH DA diffuses through the cell membrane and is enzymatically hydrolyzed by esterase to DCFH, which reacts with ROS to yield DCF. Rapid increases in DCF indicate the oxidation of DCFH by intracellular radicals. The results GSK-3 reveal that the flower extract depleted intracellular ROS in a dose dependent manner. The skin is exposed to UV and envir onmental oxidizing pollutants and is a preferred target of oxidative stress. It is reported that ultraviolet irradiation induces the formation of reactive oxygen species in cutaneous tissue, provoking toxic changes such as lipid peroxidation and enzyme inactivation. It is reported that chronic exposure to solar UV radiation plays a role in the initiation of several skin hyperpigmentation disorders.