大鼠脑缺血损伤后髓过氧化物酶的活性变化以及蒙药嘎日迪-13的干预作用

Changes of myeloperoxidase after Cerebral Ischemia in Rats and Intervention of Mongolian Medicine Garidi-13

目的:探讨脑缺血损伤后不同时相脑组织和血清中髓过氧化物酶(myeloperoxidase,MPO)的活性变化以及蒙药嘎日迪-13对其的影响。方法:取雄性SD大鼠360只,将大鼠随机分为假手术组、脑缺血模型组、嘎日迪-13大剂量组、嘎日迪-13中剂量组、嘎日迪-13小剂量5个组,每组又随机分为缺血1 h组、6 h组、12 h组、24 h组、72 h组与120 h组6个时相组,嘎日迪-13大、中、小给药组分别以1.2 g/100m L、0.6 g/100m L和0.3 g/100m L浓度2m L/100g灌胃,1次/d,连续27d后,采用改良Zea Longa线栓法制备大鼠大脑中动脉栓塞(middle cerebral artery occlusion,MCAO)模型,进行神经功能评分,在各时相规定时间点麻醉大鼠后从腹主动脉采血并取脑组织,采用分光光度法检测MPO活性。结果:与假手术组比较,脑缺血模型组各时相脑组织和血清中MPO活性都明显升高(P<0.05),具有显著性差异;与脑缺血模型组比较,嘎日迪-13大、中、小剂量组各时相脑组织和血清中MPO活性都明显降低,与模型组比较具有显著性差异(P<0.05),且24h时作用尤为明显(P<0.01)。结论:嘎日迪-13可能是通过减少脑缺血损伤后各时相MPO活性,调节各时相炎症因子相互之间的作用,减轻脑组织损伤,从而发挥对脑缺血损伤的保护作用。

Objective： To investigate the activity of myeloperoxidase （MPO） in brain tissue and serum at ent phase after cerebral ischemic in rats as well as the effect of Mongolian Medicine Gridi - 13 on them. ods ： A total of 360 male SD rats were selected. They were randomly divided into sham - operated group, group, Gridi- 13 large dose group, Gridi- 13 middle dose group and Gridi- 13 small dose group. Each differ- Meth- model group was randomLy divided into 1 h, 6 h, 12 h, 24 h, 72 h and 120 h time phase group. The middle cerebral artery occlusion （MCAO） model was established by modified Zea Longa thread - occlusion method and the activity of MPO in brain tissue and serum were analyzed by spectrophotometry. Results： Compared with the sham group, model group the activity of MPO in brain tissue and serum at different phase was significantly increased＇ （P 〈 0.05 ）, has significant differences. Garidi - 13 in each dose group could predominantly reduce the activity of MPO in brain tissue and serum at different phase, compared with model group has significant difference （P 〈 0. 05 ）. And the role of 24h is particularly evident （P 〈0.01 ）. Conclusion： Gridi- 13 could predominantly reduce the activity of MPO protect cerebral ischemia injury in rats, which may be related with alleviating neuronal damage, regulating inflammatory factors and relieving the injury of brain tissue to play a role of therapeutic action in cere- bral ischemic injury.