Objective: To investigate the effect and mechanism of anesthesia drug propofol on cerebral ischemia-reperfusion (IR) injury in rats. Methods: Seventy-two healthy male SD rats were randomly divided into sham operation group

model group

propofol (Pro) group

Pro+DPCPX group

Pro+LY294002 group

Pro+DPCPX+LY294002 group

with 12 rats in each group. The middle cerebral artery was blocked by the intravascular endothelial method

and a focal cerebral IR injury model was established. Rats were scored for neurological function 24 hours after reperfusion. Plasma levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were measured by Enzyme-linked immunosorbent assay (ELISA). The brain was detected by Triphenyl tetrazolium chloride (TTC) staining infarct volume

the expression of Bcl-2 positive cells was detected by immunohistochemistry

and the expression of Akt and p-Akt was detected by Western blot. Results: Compared with the model group

propofol effectively reduced the neurological score of IR rats and the volume of cerebral infarction

increased the expression rate of Bcl-2 positive cells in brain tissue

and effectively reduced the expression levels of plasma inflammatory factor TNF-α and IL-1β in IR rats (P<0.05). At the same time

propofol significantly increased the level of p-Akt expression in the cerebral cortex (P<0.05)

and the PI3K/Akt signaling pathway in IR rats interfered with by propofol was highly activated. When the experimental rats were treated with the PI3K in-hibitor LY294002

the neuroprotective effect of propofol was significantly inhibited and the therapy was ineffective. Its in-hibitory effect was comparable to that of A1R receptor antagonist DPCPX. Conclusion: Propofol can activate A1R in IR rat models by inhibiting the excitatory amino acid toxicity

promote the expression of p-Akt

further activate the PI3K/Akt signaling pathway

up-regulate the expression level of Bcl-2 in brain tissue

and exert anti-apoptotic effects. At the same time

it can down-regulate the expression of inflammatory factors TNF-α and IL-1β

reduce the body’s inflammatory response

and thus exerts a good therapeutic effect.