蕲蛇酶减轻大鼠局灶性脑缺血再灌注损伤的实验研究

目的:探讨蕲蛇酶(acutobin) 在局灶性脑缺血再灌注损伤模型中的保护作用及其机制。方法:线栓法制备大鼠大脑中动脉闭塞(MCAO) 模型, 缺血3 h 后恢复血流再灌24 h 。观察蕲蛇酶对脑梗死面积、脑组织中髓过氧化物酶(MPO)、诱导型一氧化氮合酶(iNOS) 活性、一氧化氮(NO)、丙二醛(MDA) 含量和超氧化物歧化酶(SOD) 活性的影响。结果:蕲蛇酶能有效减小脑梗死灶, 缓解MPO 升高、降低MDA 含量、抑制iNOS 活性, 降低NO 含量。结论:蕲蛇酶对脑缺血再灌注损伤有保护作用, 其机制可能与缓解MPO 升高以及抑制脑组织中iNOS 活性, 降低NO、MDA 含量有关。

Experimental study on alleviative effects of acutobin in treatment of focal cerebral ischemia-reperfusion injury in rats

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.