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. 2023 Nov 6;12(11):1969. doi: 10.3390/antiox12111969

Figure 3.

Figure 3

Enhancement of melanin pigmentation via NRF2 knockdown involving IFT88 and GLI1. (A) Western blot analyses depicting varying levels of tyrosinase, PMEL, and PAR2, and assays showing tyrosinase activity and melanin contents in cultured keratinocytes with NRF2 knockdown. (B–E) Western blot analyses revealing different ratios of NRF2, IFT88, GLI1, and/or tyrosinase levels in cultured keratinocytes with NRF2 knockdown in the absence and presence of SAG (B), IFT88 knockdown in the absence and presence of SAG (C), IFT88 knockdown in the absence and presence of Shh 200 (D), and GLI1 knockdown in the absence and presence of SAG (E). (F) Western blot analyses presenting different ratios of PTCH1, GLI1, GLI2, and tyrosinase levels in cultured keratinocyte–melanocyte cocultures treated with or without GANT61. β-actin served as an internal control. The data represent the means ± SD from four independent experiments. * p < 0.05, ** p < 0.01 vs. control sgRNA, # p < 0.05 vs. without SAG treatment.