Abstract: OBJECTIVE To explore the effect and its potential mechanism of sevoflurane on cerebral ischemia-reperfusion injury before and after parent artery occlusion during clipping of intracranial aneurysm.METHODS Sixty patients undergoing clipping of intracranial aneurysm were selected and randomly divided into sevoflurane group and control group. Control group adopted venous anesthesia alone, while sevoflurane group had inhaled 2% sevoflurane for 30 min before parent artery occlusion and after patency of parent artery based on venous anesthesia, respectively. The mean arterial pressure(MAP) and heart rate(HR) in both groups before parent artery occlusion(T₁), 5 min after parent artery occlusion(T₃), and 5 min after patency of parent artery(T₅) were recorded. Moreover, the jugular venous blood was collected from patients in both groups before anesthesia induction(T₀), at the time of parent artery occlusion(T₂), at the time of patency of parent artery(T₄), 2 h after patency(T₆), 6 h after patency(T₇), and 24 h after patency(T₈) to detect the beta isoform of S100 protein in astrocytes(S100β protein), tumor necrosis factor-α(TNF-α) and malondialdehyde(MDA) levels. RESULTS Differences of MAP and HR between two groups were not statistically. After parent artery occlusion, the S100β protein, TNF-α and MDA concentrations in both groups were elevated to various degrees compared with those before surgery(P<0.05); while those concentrations in sevoflurane group were lower than those in control group at T₄ and T₆-T₈(P<0.05). CONCLUSION Sevoflurane shows certain protection on cerebral ischemia-reperfusion injury, and its mechanism may be related to the suppression of excessive inflammatory response and oxidative stress response.