Propofol relieves oxidative stress response of cerebral ischemiareperfusion injury through SIRT1 signaling pathway.

This study explored the effects of propofol on the cognitive function and expressions of superoxide dismutase (SOD) and malondialdehyde (MDA) through the silent information regulator 1 (SIRT1) signaling pathway during cerebral ischemia-reperfusion (I/R) injury. C57BL/6J mice were used and divided into Sham group, I/R group (I/R model established via ligation of artery) and Treated group (peritoneal injection of propofol) according to different treatments. The memory ability of mice was evaluated using Morris water maze test, and the motor coordination was assessed using Rota rod test and oblique beam walking test. The brain tissues were prepared into embedded sections, and then the pathological changes in brain neurons were detected via hematoxylin-eosin (HE) staining, and the changes in apoptosis of brain tissues were detected via flow cytometry. Moreover, after the mice were anesthetized and sacrificed, the brain tissues were isolated and whole blood was collected. Then the changes in SIRT1 protein were determined using Western blotting, and the changes in MDA and SOD activity were determined through biochemical assays. The results of Morris water maze test and elevated plus-maze test revealed that transfer latency time (TLT) was significantly prolonged, and escape latency time (ELT) was significantly shortened in the I/R group compared with those in Sham group (*P<0.05), indicating memory impairment after cerebral I/R injury. TLT was shortened, and ELT was significantly prolonged in the Treated group compared with those in I/R group (*P<0.05). In Rota rod test, the falling down time was obviously shorter in the I/R group than in the Sham group (*P<0.05), while it was obviously longer in the Treated group than that in the I/R group (P-#<0.05). Compared with the Sham group, the I/R group had neurological impairment, manifested as the evident increase in motor performance score (*P<0.05), and the motor performance score in the Treated group was evidently lower than that in the I/R group (*P<0.05). The apoptosis was markedly enhanced in the I/R group (*P<0.05), while it was markedly weakened in the Treated group (P-#<0.05) compared with that in the Sham group. In addition, the results of Western blotting showed that the expression of SIRTI was evidently higher in I the /R group than that in the Sham group, while it evidently declined after treatment with propofol (P-#<0.05).