Autophagy Participates A? Induced Inflammatory Response In RPE Cells

Background and purpose: Dysfunction of retinal pigment epithelium(RPE)cells is associated with a variety of retinal diseases,such as age-related macular degeneration.Studies have shown that autophagy may be closely related to the inflammatory response of RPE cells,but the specific role of autophagy in the aging of RPE cells is unknown,and there is a lack of similar research.Silencing signal regulation protein 6(Sirtuin 6,SIRT6)is an important protein that regulates senility and participates in autophagy and inflammation regulation in myocardium and other tissues.Amyloid-?(A?)is the main component of drusen,a kind of pathological deposit of age-related macular degeneration,and plays an important role in the inflammatory response of RPE cells.The purpose of this study is to find the regulatory role of SIRT6 in RPE cells under the response to A?,a well-defined risk factor for retinal diseases,so as to provide new ideas for the treatment of diseases.Methods: The expression of A?,autophagy markers and SIRT6 in 3 weeks,3 months,7 months and 12 months C57BL/6 mice RPE cells were detected by immunofluorescence.A? was injected into the vitreous cavity of mice to detect the level of autophagic molecules and SIRT6.A? was added to the primary RPE cells in mice,and q PCR was used to detect the level of inflammatory factors,and tested the changes of autophagy and SIRT6.The level of autophagy was detected after si RNASIRT6 knockout and AAV-SIRT6 overexpressed ARPE-19 cells of the SIRT6 gene.PCR detected the effect of A? on the level of inflammation in the primary RPE cells of mice after the addition of 3-MA.Results: In the RPE cells of mouse eyes,A? deposition,autophagic molecules and SIRT6 are increased with age.A? promotes the expression of SIRT6 and autophagic molecules in RPE cells,and SIRT6 regulates the level of autophagy.Inhibition of autophagy weakens the inflammatory response mediated by A?.Conclusion: Autophagy regulated by SIRT6 participates in the A? mediated RPE cells inflammatory response.