Glycolic acid

Glycolic acid(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[1]

DMSO:100 mg/mL (1314.92 mM)

The effects of different concentrations of Glycolic acid(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[1].