蕲蛇酶减轻大鼠局灶性脑缺血再灌注损伤的实验研究  

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

作　　者：徐隽[1] 余涓[2] 王晶[2] 林春[2] 陈崇宏[1] 

机构地区：[1]福建医科大学药理学教研室 [2]福建医科大学生理与病理生理学系

出　　处：《中国临床药理学与治疗学》2004年第3期294-298,共5页Chinese Journal of Clinical Pharmacology and Therapeutics

基　　金：福建省自然科学基金资助课题 (№C0 0 10 0 12 )

摘　　要：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3h后恢复血流再灌 2 4h。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。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 level of NO was decreased from 17.68 ± 6.57 to 10.06 ± 4.39 μmol·g -1 pro 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 -1 pro 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 infla

关 键 词：蕲蛇酶 再灌注损伤 诱导型一氧化氮合酶 髓过氧化物酶 丙二醛 半暗带 

分 类 号：R965.1[医药卫生—药理学]