NO/H2S双供体型丁苯酞衍生物8d对大鼠脑缺血再灌注损伤的保护作用及其机制
Neuroprotective effects and mechanisms of 3-n-Butylphthalide bearing NO/H2S-donating moieties 8d against cerebral ischemia injury in rats
目的 研究经口服给予NO/H2S双供体型丁苯酞衍生物8d对大鼠脑缺血再灌注损伤的保护效应。 方法 除伪手术组外的其他各组大鼠均采用线栓法闭塞大脑中动脉（MCAO）制备大鼠局灶性脑缺血再灌注模型。通过神经功能学评分、脑梗死面积测定、脑含水量计算以及脑组织生化指标的测定来评价8d的抗脑缺血、抗脑水肿和抗氧化作用。结果 与模型组相比，8d在380mg/kg的剂量下能显著降低脑缺血再灌注损伤大鼠的神经功能学评分、缩小脑梗死面积、减少脑含水量。还具有增加脑组织中GSH含量、GSH-Px和SOD酶活力、降低脑组织MDA和ROS含量的作用；8d 在80mg/kg剂量时对脑缺血再灌注损伤的保护作用较弱。 结论 8d对大鼠脑缺血再灌注损伤具有明显的保护作用，其机制与抗氧化作用有关。
o determine the potential effects of orally administered 3-n-Butylphthalide bearing NO/H2S-donating moieties 8d on rats subjected to ischemia and reperfusion. Methods With the exception of animals in sham group, all animals in treatment groups were subjected to ischemia/reperfusion by middle cerebral artery occlusion (MCAO) with thread technique. The ability of anticerebral ischemia, relieving cerebral edema and antioxidation was evaluated by the measurement of neurological deficit score，ratios of infarction area, brain water content and brain tissu biochemical indexes related to oxidative stress in brain tissue. Results Compared with the model group, 8d(380mg/kg)can significantly reduce the neurological function, infarct size, brain water content . It also increase the the level of GSH, GSH-Px, SOD and reduce the contents of MDA and ROS. 8d (80mg/kg) has a weak protective effect against cerebralischemia. Conclusion 8d exhibited obvious protection against cerebral ischemia /reperfusion injury due to its antioxidating effect.
兰丽、吉敬、季晖
神经病学、精神病学药学基础医学
老年药理学8d脑缺血再灌注损伤大脑中动脉阻塞抗氧化
Elderly Pharmacology8dcerebral ischemia/reperfusionmiddle cerebral artery occlusion reperfusion modelsantioxidation
兰丽,吉敬,季晖.NO/H2S双供体型丁苯酞衍生物8d对大鼠脑缺血再灌注损伤的保护作用及其机制[EB/OL].(2016-04-25)[2025-07-25].http://www.paper.edu.cn/releasepaper/content/201604-321.点此复制
评论