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目的:初步研究醒脑静固体制剂对缺血性脑损伤大鼠恢复早期的保护作用及其作用机制。方法:线拴法制备永久性局灶性中动脉阻断脑缺血(pMCAO)大鼠模型,分为模型组、醒脑静12,25,50 mg.kg-1剂量组,丁苯酞(NBP)70 mg.kg-1组,ig给药12 d并设假手术组。在术后3,6,9,12,14 d,检测动物平衡能力、缺血前肢触觉、前肢肌肉张力等指标的改善状况,取材并测定动物缺血侧脑组织超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量。结果:与假手术组相比,pMCAO模型动物表现出神经功能缺损症状,在缺血后3 d横木行走评分降低65%,撕除胶布潜伏期增加13.9倍,前肢拉力减小39.7%(P<0.01)。其中,醒脑静12,25,50 mg.kg-1在缺血后6～14 d分别降低神经功能缺损评分(P<0.05或P<0.01),提高横木行走能力评分(P<0.05或P<0.01),缩短撕除潜伏期(P<0.05或P<0.01),提高前肢抓握力(P<0.05或P<0.01)。同时醒脑静可显著降低缺血侧脑组织中MDA含量(P<0.01)。结论:醒脑静固体制剂对缺血性脑损伤恢复早期大鼠模型具有一定保护作用,其作用机制可能与抑制脂质过氧化反应产物MDA含量,从而减轻氧化损伤有关。
OBJECTIVE: To study the early protective effect of xingnaojing solid preparations on rats with ischemic brain damage and its mechanism. Methods: The model of permanent focal middle artery occlusion of cerebral ischemia (pMCAO) was established by the tethering method. The rats were divided into model group, Xingnaojing 12, 25, 50 mg.kg-1 dose group, butylphthalide NBP) 70 mg.kg-1 group, ig administration for 12 days and sham operation group. At 3, 6, 9, 12, and 14 days after operation, the animals were sacrificed and the animals were sacrificed. The animals’ balance ability, the sense of forelimb ischemia and the muscle tension of the forelimb were measured. Activity and malondialdehyde (MDA) content. Results: Compared with the sham-operated group, the pMCAO model animals exhibited neurological deficits with a 65% reduction in crosswalk walking score, a 13.9-fold increase in latency and a 39.7% reduction in frontal pullout force (P <0.01) ). Among them, Xinjingjing 12, 25 and 50 mg.kg-1 decreased neurological deficit scores (P <0.05 or P <0.01) 6 to 14 d after ischemia, respectively, <0.01), shortening the tear-off latency (P <0.05 or P <0.01) and improving the grip of forelimb (P <0.05 or P <0.01). At the same time Xingnaojing can significantly reduce the ischemic brain tissue MDA content (P <0.01). Conclusion: Xingjingjing solid preparation can protect the early rat model of recovery from ischemic brain injury. The mechanism may be related to inhibiting the content of MDA in lipid peroxidation products and reducing the oxidative damage.