Abstract: AIM: To study the protective effects of acutobin on focal cerebral ischemia reperfusion injury in rats.METHODS: Reversible middle cerebral artery occlusion (MCAO) models were produced by intraluminal suture technique, and reperfusion was begun 3 h after occlusion.Acutobin was injected intravenously.After 24 h reperfusion, the infarction area was measured by using 2, 3, 5-Triphenyl tetrazolium chloride (TTC) staining.The content of nitric oxide (NO) and maleic dialdehyde (MDA), the and activities of myeloperoxidase (MPO), inducible nitric oxide synthase (iNOS) and superoxide dismutase (SOD) in brain tissue were measured.RESULTS: The infarction area was reduced by acutobin comparing with ischemia-reperfusion group.In brain tissue of the occluded side, the activity of MPO was decreased by acutobin in a dose-dependent manner, the lev-el of NO was decreased from 17.68 ±6.57 to 10.06 ± 4.39 μmol·g^-1pro by the 4 U·kg^-1 dose of acutobin administrated at the beginning of reperfusion and from 17.43 ±6.41 to 5.59 ±0.57 μmol·g^-1 pro by the 4 U·kg^-1 dose of acutobin administrated at the beginning of occlusion;the activity of iNOS was reduced from 2.11 ±0.53 to 1.17 ±0.51 U·mg^-1pro by the 4 U·kg^-1 dose of acutobin administrated at the beginning of reperfusion and from 2.10 ±0.77 to 0.58 ±0.23 U·mg^-1 pro by the 4 U·kg^-1 dose of acutobin administrated at the beginning of occlusions, and the content of MDA was reduced from 35.30 ±4.73 to 25.54 ±5.47 nmol·mg^-1 Pro by the 4 U·kg^-1 dose of acutobin administrated at beginning of reperfusion and from 34.57 ±3.47 to 18.79 ±4.99 nmol·mg^-1 Pro by the 4 U·kg^-1 dose of acutobin administrated at the beginning of occlusion.No significant effect on SOD was observed.CONCLUSION: Acutobin may protect the focal cerebral ischemia reperfusion injury by inhibiting the inflammation reaction, reducing the activity of iNOS and reducing lipid peroxides.

Key words: acutobin, reperfusion injury, inducible nitric oxide synthase, myeloperoxidase, maleic dialdehyde, ischemia penumbra