interleukin-8 and glycolic-acid

We aimed to find active substances to help relieve the symptoms caused by increased photosensitivity after alpha hydroxy acid (AHA) peeling.. A questionnaire survey was provided to 66 patients who received AHA peeling therapy to understand if increased photosensitivity existed and its specific symptoms. We verified increased photosensitivity after AHA peeling by monitoring cell viability to detect the combined toxicity of glycolic acid (GA) and UVB in HaCaT cells. The ELISA method was used to determine the expression of KLK7, FLG, IL-1β, and IL-8 to correlate damage to the skin barrier and inflammation induced by GA and UVB and the relieving effects of. Our survey results showed that 6.06% of people were more sensitive to sunlight after AHA peeling than before. Experiments at the cellular level showed that UVB induced cytotoxicity on HaCaT cells pre-treated with GA. Combined exposure of GA and UVB induced up-regulation of KLK7 and down-regulation of FLG and increased inflammatory cytokines of IL-1β and IL-8.. Our study found that combined exposure to GA and UV disrupted the skin barrier and induced significant inflammation. These results provided a theoretical basis for increased photosensitivity after chemical peeling.

Topics: Glycolates; Humans; Inflammation; Interleukin-8; Plant Extracts; Portulaca; Ultraviolet Rays

Glycolic acid (GA), commonly present in fruits, has been used to treat dermatological diseases. Extensive exposure to solar ultraviolet B (UVB) irradiation plays a crucial role in the induction of skin inflammation. The development of photo prevention from natural materials represents an effective strategy for skin keratinocytes.. The aim of this study was to investigate the molecular mechanisms underlying the glycolic acid (GA)-induced reduction of UVB-mediated inflammatory responses.. We determined the effects of different concentrations of GA on the inflammatory response of human keratinocytes HaCaT cells and C57BL/6J mice dorsal skin. After GA was topically applied, HaCaT and mice skin were exposed to UVB irradiation.. GA reduced the production of UVB-induced nuclear factor kappa B (NF-κB)-dependent inflammatory mediators [interleukin (IL)-1β, IL-6, IL-8, cyclooxygenase (COX)-2, tumor necrosis factor-α, and monocyte chemoattractant protein (MCP-1)] at both mRNA and protein levels. GA inhibited the UVB-induced promoter activity of NF-κB in HaCaT cells. GA attenuated the elevation of senescence associated with β-galactosidase activity but did not affect the wound migration ability. The topical application of GA inhibited the genes expression of IL-1β, IL-6, IL-8, COX-2, and MCP-1 in UVB-exposed mouse skin. The mice to UVB irradiation after GA was topically applied for 9 consecutive days and reported that 1-1.5% of GA exerted anti-inflammatory effects on mouse skin.. We clarified the molecular mechanism of GA protection against UVB-induced inflammation by modulating NF-κB signaling pathways and determined the optimal concentration of GA in mice skin exposed to UVB irradiation.

Topics: Administration, Cutaneous; Animals; Anti-Inflammatory Agents; Cell Line; Cell Movement; Cellular Senescence; Chemokine CCL2; Cyclooxygenase 2; Dose-Response Relationship, Drug; Glycolates; Humans; Interleukin-6; Interleukin-8; Keratinocytes; Male; Mice, Inbred C57BL; NF-kappa B; Promoter Regions, Genetic; RNA, Messenger; Signal Transduction; Skin; Time Factors; Transfection; Ultraviolet Rays