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| Study on the mechanism of Edaravone on cerebral ischemia-reperfusion injury in rats |
| MI Yan1 GAO Xiaoping2 ZHU Qingfeng2 LUO Hailong3 |
1.Department of Electrophysiology, Hu′nan Thoracic Hospital, Hu′nan Province, Changsha 410000, China;
2.Department of Neurology, Hu′nan People′s Hospital, Hu′nan Province, Changsha 410000, China;
3.Department of Endoscopic Diagnosis, Hu′nan Thoracic Hospital, Hu′nan Province, Changsha 410000, China |
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Abstract Objective To investigate the effect of Edaravone on the expression of PDCD-5 protein in rats with cerebral ischemia reperfusion. Methods Seventy-eight healthy male SD rats with a healthy weight of 250-280 g were randomly divided into blank control group (n = 6, normal saline, 3 mg/kg, twice a day, intraperitoneal injection), sham operation group (n = 24, normal saline, 3 mg/kg, twice a day, intraperitoneal injection), cerebral ischemia reperfusion group (n = 24, normal saline, 3 mg/kg, twice a day, intraperitoneal injection) and drug intervention group (n = 24, Edaravone 3 mg/kg, twice a day, intraperitoneal injection) according to random number table method, and the latter 3 groups were randomly divided into 6 h group, 1 d group, 3 d group and 7 d group. A modified Longa method was used to establish cerebral ischemia-reperfusion model. The neurological deficit, the acreage of cerebral infarction and the expression of PDCD-5 and Caspase-3 protein in hippocampus of different periods were compared. Results The cerebral infarction in cerebral ischemia reperfusion group was significantly increased compared with sham operation group (P < 0.05); the cerebral infarction in drug intervention group was significantly reduced compared with cerebral ischemia reperfusion group (P < 0.05). At the same time, the expression of PDCD-5, Caspase-3 protein in cerebral ischemia-reperfusion group at different time points was higher than those in corresponding sham-operation group and corresponding drug intervention group (P < 0.05). Conclusion Edaravone can inhibit the expression of PDCD-5 in the hippocampus of rats with cerebral ischemia-reperfusion, and protect the brain against cerebral ischemia-reperfusion injury in rats.
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