Abstract: AimTo investigate the protective effects and mechanism of action of aspirin on focal cerebral ischemia-reperfusion rats. MethodsThe right middle cerebral artery of the rat was occluded by inserting a thread through internal carotid artery for 2 h, and then reperfused for 24 h. Different doses of aspirin were intragastricly administrated at reperfusion 0 h and 6 h. The injured area of the brain and cerebral edema were estimated. The contents of prostacyclin (PGI₂), thromboxane (TXA₂), and endothelin (ET) in plasma were measured by ₁₂₅I radioimmunoassay method. The content of nitric oxide (NO) in plasma was measured by the nitrate reductase method. The malondialdehyde (MDA) content in brain tissue was determined by the thiobarbituric acid method. The superoxide dismutase content (SOD) in brain tissue was assayed by the xanthine oxidase method. The content of adenosin 5′-triphosphate (ATP) in brain tissue was separated by capillary electrophoresis. ResultsThe injured area of the brain and the cerebral edema of occluded side were drasmatically reduced after 6 and 60 mg·kg^-1 doses of aspirin were administrated intragastricaly. The ratio of PGI₂/TXA₂ in plasma was increased by aspirin in a dose-dependent manner. In brain tissue of the occluded side, the MDA content was reduced from 9.0±0.75 to 6.48±0.74, and the ATP level was increased from 10.26±1.02 to 25.65±3.45 by the 60 mg·kg^-1 dose of aspirin. No significant effect on SOD content was observed. In plasma, the NO content was significantly decreased from 24.76±1.88 to 8.17±0.79, and the ET level was increased from 254.85±21.14 to 278.43±16.79 by 6 mg·kg^-1 dose of aspirin. Conclusion The neuroprotective effects of aspirin on focal cerebral ischemia-reperfusion rats might be attributed to its effects by increasing the ratio of PGI₂ and TXA₂, reducing lipid peroxides and improving the energy metabolism.