Protective effect of oxysophoridine on cerebral ischemia/reperfusion injury in mice  

作　　者：Hongbo Wang Yuxiang Li Ning Jiang Xiaoping Chen Yi Zhang Kuai Zhang Tengfei Wang Yinju Hao Lin Ma Chengjun Zhao Yanrong Wang Tao Sun Jianqiang Yu 

机构地区：[1]Department of Pharmacology, Ningxia Medical University [2]College of Nursing, Ningxia Medical University [3]Shanghai Pudong New Area Gongli Hospital [4]Ningxia Key Laboratory of Craniocerebral Diseases of Ningxia Hui Autonomous Region [5]School of Basic Medical Sciences, Ningxia Medical University [6]Key Laboratory of Reproduction and Genetics of Ningxia Medical University [7]Collaborative Innovation Center of Ningxia Hui Autonomous Region for Medicines

出　　处：《Neural Regeneration Research》2013年第15期1349-1359,共11页中国神经再生研究（英文版）

基　　金：supported by the National Natural Science Foundation of China, No. 30960506, 81160524;the Natural Science Foundation of Ningxia Hui Autonomous Region, No. NZ11212;the Key Scientific Research Project of Ningxia Hui Autonomous Region Health Department, No. 2012152;the Project of Ningxia Medical University, No. XM2011017

摘　　要：Oxysophoridine, a new alkaloid extracted from Sophora alopecuroides L., has been shown to have a protective effect against ischemic brain damage. In this study, a focal cerebral ischemia/reperfusion injury model was established using middle cerebral artery occlusion in mice. Both 62.5, 125, and 250 mg/kg oxysophoridine, via intraperitoneal injection, and 6 mg/kg nimodipine, via intragastric administration, were administered daily for 7 days before modeling. After 24 hours of reperfusion, mice were tested for neurological deficit, cerebral infarct size was assessed and brain tissue was collected. Results showed that oxysophoridine at 125, 250 mg/kg and 6 mg/kg nimodipine could reduce neurological deficit scores, cerebral infarct size and brain water content in mice. These results provided evidence that oxysophoridine plays a protective role in cerebral ischemia/reperfusion injury. In addition, oxysophoridine at 62.5, 125, and 250 mg/kg and 6 mg/kg nimodipine increased adenosine-triphosphate content, and decreased malondialdehyde and nitric oxide content. These compounds enhanced the activities of glutathione-peroxidase, superoxide dismutase, catalase, and lactate dehydrogenase, and decreased the activity of nitric oxide synthase Protein and mRNA expression levels of N-methyI-D-aspartate receptor subunit NR1 were markedly inhibited in the presence of 250 mg/kg oxysophoridine and 6 mg/kg nimodipine. Our experimental findings indicated that oxysophoridine has a neuroprotective effect against cerebral ischemia/reperfusion injury in mice, and that the effect may be due to its ability to inhibit oxidative stress and expression of the N-methyI-D-aspartate receptor subunit NR1.Oxysophoridine, a new alkaloid extracted from Sophora alopecuroides L., has been shown to have a protective effect against ischemic brain damage. In this study, a focal cerebral ischemia/reperfusion injury model was established using middle cerebral artery occlusion in mice. Both 62.5, 125, and 250 mg/kg oxysophoridine, via intraperitoneal injection, and 6 mg/kg nimodipine, via intragastric administration, were administered daily for 7 days before modeling. After 24 hours of reperfusion, mice were tested for neurological deficit, cerebral infarct size was assessed and brain tissue was collected. Results showed that oxysophoridine at 125, 250 mg/kg and 6 mg/kg nimodipine could reduce neurological deficit scores, cerebral infarct size and brain water content in mice. These results provided evidence that oxysophoridine plays a protective role in cerebral ischemia/reperfusion injury. In addition, oxysophoridine at 62.5, 125, and 250 mg/kg and 6 mg/kg nimodipine increased adenosine-triphosphate content, and decreased malondialdehyde and nitric oxide content. These compounds enhanced the activities of glutathione-peroxidase, superoxide dismutase, catalase, and lactate dehydrogenase, and decreased the activity of nitric oxide synthase Protein and mRNA expression levels of N-methyI-D-aspartate receptor subunit NR1 were markedly inhibited in the presence of 250 mg/kg oxysophoridine and 6 mg/kg nimodipine. Our experimental findings indicated that oxysophoridine has a neuroprotective effect against cerebral ischemia/reperfusion injury in mice, and that the effect may be due to its ability to inhibit oxidative stress and expression of the N-methyI-D-aspartate receptor subunit NR1.

关 键 词：neural regeneration traditional Chinese medicine brain injury OXYSOPHORIDINE ischemia/reperfusion injury oxidative stress N-methyI-D-aspartate receptor NEUROPROTECTION grants-supported paper NEUROREGENERATION 

分 类 号：R285.5[医药卫生—中药学]