尤瑞克林对H2O2诱导的海马神经元损伤的保护作用研究
合集下载
- 1、下载文档前请自行甄别文档内容的完整性，平台不提供额外的编辑、内容补充、找答案等附加服务。
- 2、"仅部分预览"的文档,不可在线预览部分如存在完整性等问题,可反馈申请退款(可完整预览的文档不适用该条件!)。
- 3、如文档侵犯您的权益，请联系客服反馈,我们会尽快为您处理(人工客服工作时间：9:00-18:30)。
国际医药卫生导报2019年第25卷第8期IMH(；N. April 2019, \ «1.25 No. 8
•科研课题•
尤瑞克林对h2o2诱导的海马神经元损伤的
保护作用研究
廖劭伟'胡雅纯2李怡I余群］范胜诺'刘军I I中山大学孙逸仙纪念医院神经科，广州510120; 2 r州市惠爱医院脑电图室510370; '中山大学孙逸仙纪念医院康复医学科，广州510120 通信作者：刘军，Email: dodiujun@
【关键词］尤瑞克林；氧化应激；ERK 基金项目：国家自然科学基金( 81870836 ):天普研究基金(KF201405 )
D01: 10.3760/cma.j.issn. 1007-1245.2019.08.002
Protective effect of urinapocampal neuron injury
[Abstract ] Objective To study the protective effect of urinary kallindinogenase (UK) on oxidative stress injury in hippocampal neurons. Methods HT22 cells were treated with H2O2 to construct oxidative stress injury cell model. CCK-8 method was used to detect the effect of UK on the viability of H2O2 injured HT22 cells. H2DCF-DA essay was conducted to determine the impact of UK on reactive oxygen species (ROS) in HT22 cells after H2O2 treatment. The phosphorylation level of ERK and the expression of Cleaved-Caspase 3 in UT22 cells were detected by Western blot after H2O2 treatment, with or without UK. Results Conipared with the control group, the viability of HT22 cells decreased gradually with the in crease of H2O2 concen tration (P<0.05). Furthermore, ROS level, ERK phosphorylation level, and the expression of Cleaved-Caspase 3 were also upregulated (P<0.05). UK did not affect the HT22 cell viability in the certain concentration range (<500 nM) (P>0.05). When H2O2 was co-incubated with UK, the viability of HT22 cells increased as the concentration of UK raised in the certain range (P<0.05), while ROS content, ERK phosphorylation level, and Cleaved-Caspase 3 expression were significantly down-regulated (P<0.05). Conclusion UK shows potent protection on neuronal oxidative stress injury, in which ERK pathway may be invoIved.
Liao Shaowei1, Hu Yachun2, Li Yi', Yu Qun', Fan Shengnuo ', Lin Jun1 'Department of Neurology', Sun Yat-sen Memorial Hospital. Sun Yat-sen University, Guangzhou 51012(), China; Department of EEG, Guangzhou Huicii Hospital. Guangzhou 5103 7(), China; Department of Rehabilitation Medicine, Sim Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China Corresponding author: Liu Jun, Email: docliujun@
【摘要］目的 研究尤瑞克林(urinary kallindinogenase, I K )对海马神经兀氧化应激损伤的保护 作用"方法 以比。2干预HT22细胞构建神经元氧化应激损伤模型,CCK-8法检测UK对HQ?损伤后 HT22细胞活力的影响,H2DCF-DA法测定I K对H。损伤后HT22细胞内活性氧(ROS )的水平的影响. Western 1>1<>|法检测UK对H,(),损伤后H T22细胞ERK的磷酸化水平、Oeave.l-Caspase 3农达的影响 结 果 相较于对照组，随着H;(),浓度升高，H T22活力逐渐下降(P < 0.05 ) , ROS水平升高(P < 0.05 ), EBK磷酸化水平升高(P < 0.05 ) , (：leave<l-Caspase 3表达上调(P < 0.05 ) ; UK在较高浓度范围内 (W 500 nM )对细胞活力无明显影响(P > 0.05 )；而H：()：与UK共孵育时，HT22细胞活力随着I K浓 度升高而逐渐改善(P < 0.05 ) , BOS水平显著下降(P < 0.05 ) , KRK磷酸化水平明显降低(P < 0.05 ), Cleaved-Caspase 3表达®.著下调(P < ().05 )结论「K对神经尤氣化应激损伤具有保护作用.其可能 与ERK通路的参与有关：
•科研课题•
尤瑞克林对h2o2诱导的海马神经元损伤的
保护作用研究
廖劭伟'胡雅纯2李怡I余群］范胜诺'刘军I I中山大学孙逸仙纪念医院神经科，广州510120; 2 r州市惠爱医院脑电图室510370; '中山大学孙逸仙纪念医院康复医学科，广州510120 通信作者：刘军，Email: dodiujun@
【关键词］尤瑞克林；氧化应激；ERK 基金项目：国家自然科学基金( 81870836 ):天普研究基金(KF201405 )
D01: 10.3760/cma.j.issn. 1007-1245.2019.08.002
Protective effect of urinapocampal neuron injury
[Abstract ] Objective To study the protective effect of urinary kallindinogenase (UK) on oxidative stress injury in hippocampal neurons. Methods HT22 cells were treated with H2O2 to construct oxidative stress injury cell model. CCK-8 method was used to detect the effect of UK on the viability of H2O2 injured HT22 cells. H2DCF-DA essay was conducted to determine the impact of UK on reactive oxygen species (ROS) in HT22 cells after H2O2 treatment. The phosphorylation level of ERK and the expression of Cleaved-Caspase 3 in UT22 cells were detected by Western blot after H2O2 treatment, with or without UK. Results Conipared with the control group, the viability of HT22 cells decreased gradually with the in crease of H2O2 concen tration (P<0.05). Furthermore, ROS level, ERK phosphorylation level, and the expression of Cleaved-Caspase 3 were also upregulated (P<0.05). UK did not affect the HT22 cell viability in the certain concentration range (<500 nM) (P>0.05). When H2O2 was co-incubated with UK, the viability of HT22 cells increased as the concentration of UK raised in the certain range (P<0.05), while ROS content, ERK phosphorylation level, and Cleaved-Caspase 3 expression were significantly down-regulated (P<0.05). Conclusion UK shows potent protection on neuronal oxidative stress injury, in which ERK pathway may be invoIved.
Liao Shaowei1, Hu Yachun2, Li Yi', Yu Qun', Fan Shengnuo ', Lin Jun1 'Department of Neurology', Sun Yat-sen Memorial Hospital. Sun Yat-sen University, Guangzhou 51012(), China; Department of EEG, Guangzhou Huicii Hospital. Guangzhou 5103 7(), China; Department of Rehabilitation Medicine, Sim Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China Corresponding author: Liu Jun, Email: docliujun@
【摘要］目的 研究尤瑞克林(urinary kallindinogenase, I K )对海马神经兀氧化应激损伤的保护 作用"方法 以比。2干预HT22细胞构建神经元氧化应激损伤模型,CCK-8法检测UK对HQ?损伤后 HT22细胞活力的影响,H2DCF-DA法测定I K对H。损伤后HT22细胞内活性氧(ROS )的水平的影响. Western 1>1<>|法检测UK对H,(),损伤后H T22细胞ERK的磷酸化水平、Oeave.l-Caspase 3农达的影响 结 果 相较于对照组，随着H;(),浓度升高，H T22活力逐渐下降(P < 0.05 ) , ROS水平升高(P < 0.05 ), EBK磷酸化水平升高(P < 0.05 ) , (：leave<l-Caspase 3表达上调(P < 0.05 ) ; UK在较高浓度范围内 (W 500 nM )对细胞活力无明显影响(P > 0.05 )；而H：()：与UK共孵育时，HT22细胞活力随着I K浓 度升高而逐渐改善(P < 0.05 ) , BOS水平显著下降(P < 0.05 ) , KRK磷酸化水平明显降低(P < 0.05 ), Cleaved-Caspase 3表达®.著下调(P < ().05 )结论「K对神经尤氣化应激损伤具有保护作用.其可能 与ERK通路的参与有关：