Dexmedetomidine regulates the anti-oxidation and autophagy of adipose-derived stromal cells under H2O2-induced oxidative stress through Nrf2/p62 pathway and improves the retention rate of autologous fat transplantation

To investigate the protective mechanism of dexmedetomidine (DEX) on adipose-derived stromal cells (ADSCs) under oxidative stress model and its promotion effect on the retention rate of adipose granule transplantation by <i>in vitro</i> and <i>in vivo</i> experiments. The experiment was divided into control group, model group (ADSCs + H₂O₂+normal serum), DEX group (ADSCs + H₂0₂+DEX drug-containing serum), autophagy agonist group (ADSCs + H₂O₂+rapamycin (RAP)+normal serum), RAP + DEX group (ADSCs + H₂O₂+normal serum), RAP + DEX drug-containing serum), autophagy inhibitor group (ADSCs + H₂O₂+chloroquine (CQ)+normal serum), CQ + DEX group (ADSCs + H₂O₂+CQ + DEX drug-containing serum). HO-1, GSH-PX, SOD and CAT in ADSCs under oxidative stress model were measured. ROS fluorescence intensity and apoptosis ratio were detected. Expression of Nrf2, LC3-II/LC3-I and p62 were detected. <i>In vivo</i>, fat mixed with ADSCs or DEX -pretreated ADSCs was implanted subcutaneously in the lower back region of nude mice. Fat grafts were collected and analyzed at 2-, 4-, 6-, and 8-weeks post-transplantation. DEX pretreatment could reduce the expression of p62 to enhance the autophagy level of ADSCs under oxidative stress model. Additionally, cotransplantation of DEX-pretreated ADSCs with fat improved the long-term texture of fat grafts. DEX increased the fat graft survival and angiogenesis.