Anti-glycation activities of methyl gallate in vitro and in human explants

Background The build-up of advanced glycation end products (AGEs) is one of important factor of skin aging. Natural compounds with anti-glycation activities might have great anti-aging potential. Aims The objective of this study was to evaluate an anti-glycation effects of methyl gallate as a potent ingredient for anti-aging. Methods We first evaluated the AGEs inhibitory ability of methyl gallate in BSA/glucose system. Levels of N epsilon-CML and carbonyl contents were also measured in BSA/glucose system. To further investigate if methyl gallate could prevent glycation in full-thickness human skin explants. Glycation action was determined by the observation of the general morphology of dermis and epidermis structures and FBN-1 and of CML immunostaining. In an in-vivo study, primary irritation test was also performed to ensure the safety of methyl gallate for human skin. Results It is known that methyl gallate can suppress glycation reaction between BSA and glucose. Methyl gallate also has a remarkable potential to reduce the oxidation of proteins. Furthermore, the anti-glycation activity of methyl gallate has been confirmed in a human skin ex-vivo model. Methyl gallate decreased the expression of CML but stimulated the expression of FBN-1 compared with MGO treatment. In an in-vivo study, methyl gallate (0.1%) did not cause any skin irritation, suggesting that methyl gallate could be used as an active ingredient in cosmetics. Conclusion Our results showed that methyl gallate could protect against glucose-mediated glycation in vitro. Furthermore, methyl gallate significantly prevented glycation in living human skin explants. Due to these beneficial effects, methyl gallate can be used to prevent or manage AGE-mediated skin aging.

Automated summary

Methyl gallate demonstrated anti-glycation and antioxidant potential, validated in a human skin ex-vivo model. It did not cause skin irritation and can be used as an active ingredient in cosmetics.