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表儿茶酸激活Nrf2/ARE通路在小鼠脑外伤中的神经保护作用 被引量:3

Neuroprotective effects of(-)-epicatechin on traumatic brain injury mice by nuclear factor E2-related factor 2 pathway
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摘要 目的探讨表儿茶酸(EC)对脑损伤(TBI)小鼠的神经的神经保护作用.方法采用自由落体法制备TBI小鼠模型,将小鼠随机分为假手术(Sham)组,脑损伤+盐水(TBI+Veh)组和脑损伤+表儿茶酸(TBI+EC)组.术后3d,蛋白质印迹法(Western blot)检测Nrf2、SOD1和NQO1的表达.术后28 d,小鼠大脑损伤体积.术后7、28 d,观察小鼠神经功能缺损评分(NDS),挂线实验,评价小鼠的运动功能,悬尾实验和强迫游泳实验评价小鼠抑郁情绪状况.结果术后3d,EC治疗组细胞核中Nrf2表达量(1.354±0.432)明显高于盐水组(0.847±0.345),EC治疗组细胞中SOD1和NQO1的表达量[(1.128±0.326)和(1.325±0.427)]明显高于盐水[(0.847±0.365)和(1.025±0.317),P<0.05].NDS评分结果显示EC治疗组第7天和第28天后肢运动功能评分[(7.18±1.26)和(3.25±0.91)]与Veh组比较[(9.75±1.16)和(6.63±1.06),P<0.05],明显降低.挂线实验结果显示EC治疗组第7天和第28天挂线时间[(22.48±2.26)和(45.35±2.92)]与Veh组比较[(12.23±2.11)和(22.53±2.32),P<0.05]明显增加.术后28 d,在悬尾实验和强迫游泳实验中,EC治疗组的不动时间为[(202.88±12.56)和(101.98±22.43)],较Veh组[(244.48±22.76)和(145.39±19.86)]比较明显降低,差异有统计学意义.对比Veh组,EC组28 d损伤体积(8.95±1.59)mm3明显低于Veh组[(11.52±1.17)mm3,P<0.01].结论颅脑外伤后,EC对通过激活Nrf2通路起神经保护作用. Objective To investigate the neuroprotective effect of(-)-epicatechin(EC)on traumatic brain injury(TBI)mice.Methods TBI mouse model was prepared by modified weight drop method.Animals were randomly divided into Sham group,TBI+Veh group and TBI+EC group.At 3 days after TBI,Western blotting was used to detect the expression of Nr£2,SOD1 and NQO1.On days 7 and 28 post TBI,Neurologic deficit score(NDS)and wire hanging test were used to detect the motor function.Tail suspension test and forced swim test were used to evaluate the depressive status of mice after TBI on day 28.Results(1)Compared with Veh group,the expression of Nrf2 in nudes was obviously higher(1.354±0.432 vs.0.847±0.345)in EC treated group.The expression of SOD1 and NQO1(1.128±0.326)and(1.325±0.427),P<0.05)was significantly increased,compared with them in the Veh group[(0.855±0.365)and(1.025±0.317)].NDS showed that EC treatment group on 7 d and 28d scores of motor function[(7.18±1.26)and(3.25±0.91)]significantly improved,compared with the Veh Group[(9.75±1.16)and(6.63±1.06),P<0.05].In the wire hanging test,the mice in EC group have more latency time(22.48±2.26)s and(45.35±2.92)s]compared to让in the Veh group[(12.23±2.11)s and(22.53±2.32)s,P<0.05]on day 7 and 28 post TBI.(3)On day 28,in the tail suspension test and force swim test,the immobility time in the EC treated group[(202.88±12.56)and(101.98±22.43)]is shorter than it in the vehicle treated group[(244.48±22.76)and(145.39±19.86),P<0.05].(4)On day 28 post injury,compared with the Veh group,the lesion volume is smaller in the EC treatd group[(8.95±1.59)mm^3 vs.(11.52±1.17)mm3,P<0.01].Conclusion EC protects the brain after TBI by NRf2 pathway.
作者 陈向荣 寇红伟 包德明 孙新志 刘宏建 程田 王义生 Chen Xiangrong;Kou Hongwei;Bao Deming;Sun Xinzhi;Liu Hongjian;Cheng Tian;Wang Yisheng(Department of Orthopedics,the First Affiliated Hospital of Zhengzhou University,Zhengzhou 450052,China)
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2019年第12期2224-2226,共3页 Chinese Journal of Experimental Surgery
关键词 表儿茶酸 脑外伤 神经保护 (-)-epicatechin Traumatic brain injury Neuroprotection
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