RESUMEN
The advanced glycation end-products (AGEs) are produced through non-enzymatic glycation between reducing sugars and free amino groups, such as proteins, lipids or nucleic acids. AGEs can enter the body through daily dietary intake and can also be generated internally via normal metabolism and external stimuli. AGEs bind to cell surface receptors for AGEs, triggering oxidative stress and inflammation responses that lead to skin ageing and various diseases. Evidence shows that AGEs contribute to skin dysfunction and ageing. This review introduces the basic information, the sources, the metabolism and absorption of AGEs. We also summarise the detrimental mechanisms of AGEs to skin ageing and other chronic diseases. For the potential strategies for counteracting AGEs to skin and other organs, we summarised the pathways that could be utilised to resist glycation. Chemical and natural-derived anti-glycation approaches are overviewed. This work offers an understanding of AGEs to skin ageing and other chronic diseases and may provide perspectives for the development of anti-glycation strategies.
Asunto(s)
Reacción de Maillard , Piel , Humanos , Estrés Oxidativo , Enfermedad CrónicaRESUMEN
Our skin is an organ with the largest contact area between the human body and the external environment. Skin aging is affected directly by both endogenous factors and exogenous factors (e.g., UV exposure). Skin saccharification, a non-enzymatic reaction between proteins, e.g., dermal collagen and naturally occurring reducing sugars, is one of the basic root causes of endogenous skin aging. During the reaction, a series of complicated glycation products produced at different reaction stages and pathways are usually collectively referred to as advanced glycation end products (AGEs). AGEs cause cellular dysfunction through the modification of intracellular molecules and accumulate in tissues with aging. AGEs are also associated with a variety of age-related diseases, such as diabetes, cardiovascular disease, renal failure (uremia), and Alzheimer's disease. AGEs accumulate in the skin with age and are amplified through exogenous factors, e.g., ultraviolet radiation, resulting in wrinkles, loss of elasticity, dull yellowing, and other skin problems. This article focuses on the damage mechanism of glucose and its glycation products on the skin by summarizing the biochemical characteristics, compositions, as well as processes of the production and elimination of AGEs. One of the important parts of this article would be to summarize the current AGEs inhibitors to gain insight into the anti-glycation mechanism of the skin and the development of promising natural products with anti-glycation effects.
Asunto(s)
Insuficiencia Renal , Envejecimiento de la Piel , Humanos , Productos Finales de Glicación Avanzada/metabolismo , Rayos Ultravioleta/efectos adversos , Piel/metabolismo , Glicosilación , Insuficiencia Renal/metabolismoRESUMEN
BACKGROUND: The accumulation of advanced glycation end products has been proposed as a causative agent of skin aging, but there are no conventional devices for quantifying advanced glycation end-product accumulation in facial skin. AIMS: This study aimed to develop a convenient and accurate in situ advanced glycation end-product measurement system for the human face. METHODS: We developed a facial glycation imaging system, which consisted of illumination (white light-emitting diode, ultraviolet light-emitting diode) and image acquisition modules to capture face images. Advanced glycation end product-related autofluorescence and total skin reflectance were calculated to obtain the skin glycation index using an image analysis algorithm. Correlations between the skin glycation index and facial skin elasticity and age were examined in 36 healthy Korean women. RESULTS: The facial glycation imaging system was validated against a volar forearm skin autofluorescence measurement device, that is, the AGE Reader mu, with forearm skin glycation index (R = 0.64, P < .01). Cheek elasticity was negatively correlated with cheek skin glycation index (R = -0.56, R = -0.57, and R = -0.61, P < .01 for R2, R5, and R7, respectively). Age was significantly correlated with forearm skin glycation index (R = 0.44, P < .01) and cheek skin glycation index (R = 0.48, P < .01). CONCLUSION: We successfully developed a novel in situ facial skin glycation index measurement device. Our convenient and accurate system enables in situ skin glycation index monitoring for skin aging studies such as those on anti-glycation cosmetics.