Abstract: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.
