Abstract:

The aim of the study was to investigate the regulatory effect and mechanism of chlorogenic acid （CGA） on UVB-induced inflammatory response in HaCaT cells. HaCaT cells exposed to UVB were treated with CGA, and the protective effect of CGA on HaCaT cells damaged by UVB was detected by crystal violet staining. Changes in intracellular TNF-α content were detected by enzyme-linked immunosorbent assay, the antioxidant capacity of CGA in and out of the cells was detected by ABTS, DPPH, and FRAP assay, MDA content in the cells was detected by malondialdehyde kit, changes in total intracellular reactive oxygen species were detected by CM-H2DCFDA staining, and the relative expression of SIRT6, TNF-α, P-AKT, P-AMPK, AMPK, β-Tubulin proteins were detected by Western blot assay. Crystal violet staining and microscopy indicate that 100 and 150 μmol/L CGA are protective for 21.6 mJ/cm² UVB-treated HaCaT cells. Enzyme-linked immunosorbent assay results indicate that CGA treatment significantly reduces TNF-α expression （P<0.01）. CGA has good free radical scavenging ability both inside and outside cells, and is able to effectively reduce the UVB induced production of MDA and ROS. CGA can significantly inhibit the upregulation of SIRT6 expression caused by UVB, thereby reducing the phosphorylation level of AKT, activating AMPK and then reducing the expression of TNF-α, and alleviating the inflammatory response of the cells. CGA can inhibit SIRT6 to reduce the inflammatory response of UVB-induced HaCaT cells and reduce UVB-inflicted cellular oxidative stress with strong anti-cutaneous photoaging activity.

Key words: chlorogenic acid, SIRT6, TNF-α, inflammation, skin photoaging