依达拉奉对血管性痴呆大鼠认知功能损害的保护作用

Edaravone enhances clearance of free radicals in vascular dementia rats and improves behavioral deficits

目的观察依达拉奉对血管性痴呆大鼠认知功能损伤的保护作用。方法将10周龄Wistar大鼠48只随机分为正常组(N组,6只)、假手术组(S组,6只)、痴呆模型组(M组18只)、依达拉奉治疗组(MT组,18只),然后再将M和MT组随机分成缺血2、4、8周组,每组6只。在完成穿梭箱、水迷宫实验测试后,断头取脑,分别检测脑组织和血清中超氧化物歧化酶(SOD)、过氧化脂质(LPO)、谷胱甘肽过氧化物酶(GSH-PX)和丙二醛(MDA)的变化。结果 M、MT组大鼠的学习和记忆潜伏期、主动逃避次数与S、N组大鼠比较差异有统计学意义(P<0.01);MT组大鼠的学习和记忆潜伏时间显著缩短,主动逃避次数显著增多,与M组间差异有统计学意义(P<0.01);M组大鼠前后2次跳台实验结果比较差异无统计学意义。生化检测发现MT组MDA、LPO表达较M组降低,差异有统计学意义(P<0.05),MT组SOD、GSH-PX表达较M组增高,差异有统计学意义(P<0.05);MT组SOD、MDA、GSH-PX、LPO表达较N、S组增高,差异有统计学意义(P<0.05);M组SOD、MDA、GSH-PX、LPO表达较N、S组增高,差异有统计学意义(P<0.01)。结论依达拉奉能降低血管性痴呆大鼠脑组织和血清中MDA、LPO水平,增强SOD、GSH-PX表达,提示依达拉奉可能通过清除血管性痴呆大鼠自由基、抑制氧化应激效应发挥脑保护作用。

Objective To investigate the edaravone influences on behaviour and expression of superoxide dismutase（SOD）,matondialdehyde（MDA）,glutathione peroxidase（GSH-PX）,lipid peroxidation（LPO）,for in vascular dementia brain.Methods Wistar rats were randomly divided into：normal group（N）,sham group（S）,vascular dementia model group（M） and edaravone treatment groups（MT）.Serum level and brain tissue expression of SOD,MDA,GSH-PX,LPO was measured by biochemistry.Results The memory and learn latent phase,activeavodiance response of M and MT group was statistics difference when compared with S and N group（P〈0.01）.The difference also existed in M and MT group（P〈0.01）.MT had shorten latent phase and more activeavoidance response.The results of M group HAD statistic difference before and after step down test.The serum level and expression of MDA,GSH-PX,LPO in MT group were lower than those in M group（P〈0.05）,the serum level and expression of SOD in MT group were higher than those in M group（P〈0.05）;the serum level and expression of SOD,MDA,GSH-PX,LPO in MT and M groups were higher than those in N,S groups（P〈0.01）.Conclusion Edaravone can restrain the expression of MDA and LPO,and increase the expression of SOD and GSH-PX in vascular dementia.Edaravone can enhance clearance of free radicals to protect neural function by restraining oxidative stress.