Objectives: Pine bark extract inhibits the induction of melanin production by melanocytes after ultraviolet, visible light, and infrared radiation.
An in vitro study was performed to evaluate the Pinus bark extract activity on human melanocyte cultures by measuring the synthesis of melanin, tyrosinase, endothelin-1, and PPAR, under the action of ultraviolet radiation A (UVA) and B (UVB), infrared-A radiation (IRA), and visible light (VL).
Introduction: Botanical extracts, such as pine bark extract, have been studied for its bleaching action due to its antioxidant, anti-inflammatory, and supposedly-granted antimelanogenic activity. In addition, many efforts have been made to elucidate its possible etiopathogenic mechanisms involved in hyperpigmentation processes, such as the production of endothelin-1 and increased tyrosinase activity, which consequently lead to melanin production. Further, the genes involved in peroxisome proliferator-activating receptor signaling cascade (PPAR) seems to be downregulated.
Materials / method: Human melanocytes were seeded and incubated with a dry extract solution of Pinus pinaster, after determination of the non-cytotoxic concentrations, and exposed to UVA/UVB, IRA, and VL, as well as the association of the radiations. Subsequently, quantification of melanin concentration, tyrosinase activity, endothelin-1, and PPAR mediators was performed.
Results: Pine bark extract reduced melanin synthesis up to 7.66, 5.14, and 4.05% when compared to UVA/UVB, IRA, and association radiation, respectively. In relation to the activity of the enzyme tyrosinase, Pycnogenol® achieved approximately a 66.5% reduction in enzymatic activity and showed reductions in the synthesis of endothelin-1 by up to 56.47, 59.33, 58.00, and 73.03% when compared to UVA/UVB, IRA, VL, and association radiation, respectively. The synthesis of PPAR was reduced up to 38.41, 26.39, 19.51, and 56.44% when compared to UVA/UVB, IRA, VL, and association radiation, respectively.
Conclusion: Pine bark extract reduces the production of melanic pigmentation by downregulating tyrosinase, endothelin-1, and PPAR synthesis.
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