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苦参碱对大鼠脑缺血/再灌注损伤的保护作用

Protective effects of matrine on cerebral ischemia/reperfusion injury in rats
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摘要 目的探讨苦参碱对缺血/再灌注脑损伤大鼠的保护作用及其可能的作用机制。方法通过颈总动脉栓线造成大脑中动脉缺血,缺血2h后将栓线拔出以实现大脑中动脉血流再灌注,120只sD大鼠随机分为假手术组、模型组、苦参碱50mg·kg^-1组、苦参碱25mg·kg^-1组、苦参碱12.5mg·kg^-1组和尼莫地平组,观察苦参碱对大鼠神经症状、脑梗死范围、脑含水量以及对缺血侧脑组织匀浆超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量及乳酸脱氢酶(LDH)活力的影响。对脑组织进行病理组织切片检查。结果苦参碱能明显改善脑缺血/再灌注损伤24h后大鼠的神经行为学评分,与模型组相比,苦参碱(50、25mg·kg^-1)组能明显减小大鼠脑梗死范围,降低脑含水量,SOD活力明显增高,苦参碱各组LDH活力和MDA水平明显降低,脑组织病理切片也证实了该药对神经细胞的保护作用。结论苦参碱对大鼠缺血/再灌注脑损伤有保护作用,该作用可能与其升高SOD活力、降低MDA含量及LDH活力有关。 Objective To observe the protective effects of matrine on cerebral ischemia/reperfusion injury in rats and explore its mechanism. Methods Cerebral ischemia/reperfusion injury in rats was induced by middle cerebral artery occlusion. The neurological outcome, infarct size and water contents were evaluated. SOD and LDH activity, MDA levels of ischemia cerebral tissue were measured. The pathomorphology examination was done. Results Matrine improved neu- rologie defects in 24 h reperfusion rats. Matrine ( 50, 25 mg·kg^-1 ) markedly decreased infarct size and edema in rats. SOD activity in matrine (50, 25 mg·kg^-1 ) groups was higher, and LDH activity and MDA level in Matrine (50, 25, 12.5 mg·kg^-1) groups were significantly lower than those in vehicle group. The pathological slices also proved its pro- tective effect on neuron cells. Conclusions Matrine has protective effects on cerebral ischemia/reperfusion injury in rats. Its role is probably related to its effect on the activity of SOD and LDH, and the level of MDA.
出处 《徐州医学院学报》 CAS 2012年第12期830-833,共4页 Acta Academiae Medicinae Xuzhou
关键词 苦参碱 脑缺血 再灌注损伤 matrine cerebral ischemia reperfusion injury
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参考文献3

  • 1Longa EZ,Weinstein PR,Carlson S. Reversible middle cerebral artery occlusion without craniectomy in rats[J].Stroke,1989,(01):84-91.
  • 2Bederson JB,Pitts LH,Tsuji M. Rat middle cerebral artery occlusion:evaluation of the model and development of a neurologic examination[J].Stroke,1986,(03):472-476.
  • 3Kristián T,Siesj(o) BK. Calcium-related damage in ischemia[J].Life Sciences,1996,(5-6):357-367.

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