[1]张杰 李易易 张兆辉.溶血磷脂酸诱导PC12细胞凋亡的机制研究[J].卒中与神经疾病杂志,2019,26(03):255-260.[doi:10.3969/j.issn.1007-0478.2019.03.001]
　Zhang Jie,Li Yiyi,Zhang Zhaohui.A study on mechanism of lysophosphatidic acid induced apoptosis of PC12 cells[J].Stroke and Nervous Diseases,2019,26(03):255-260.[doi:10.3969/j.issn.1007-0478.2019.03.001]
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溶血磷脂酸诱导PC12细胞凋亡的机制研究()
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《卒中与神经疾病》杂志[ISSN:1007-0478/CN:42-1402/R]

卷:
第26卷
期数:
2019年03期
页码:
255-260
栏目:
论 著
出版日期:
2019-06-25

文章信息/Info

Title:
A study on mechanism of lysophosphatidic acid induced apoptosis of PC12 cells
文章编号:
1007-0478(2019)03-0255-06
作者:
张杰 李易易 张兆辉
430060 武汉大学人民医院神经内科[张杰 李易易 张兆辉(通信作者)]
Author(s):
Zhang Jie;  Li Yiyi;  Zhang Zhaohui
Department of Neurology, Renmin Hospital of Wuhan University, Wuhan 430060
关键词:
溶血磷脂酸 PC12 JNK 凋亡
Keywords:
Lysophosphatidic acid PC12 JNK Apoptosis
分类号:
R742
DOI:
10.3969/j.issn.1007-0478.2019.03.001
文献标志码:
A
摘要:
目的 探究溶血磷脂酸诱导PC12细胞凋亡的机制并提出干预措施。方法 实验1:不同浓度LPA(0 μM 、10 μM、20 μM、40 μM)处理PC12细胞24 h; 实验2:LPA(40 μM)分别处理PC12细胞不同时间(0 h、6 h、12 h、24 h); 实验3:正常组(0 μM LPA)、LPA组(40 μM LPA)和干预组(5 μM SP600125预处理2 h+40 μM LPA)培养24 h; CCK-8检测细胞活力; TUNEL染色检测细胞凋亡比例; WesternBlot检测Bcl2、caspase 3、磷酸化JNK水平。结果 LPA以时间依赖和浓度依赖的方式使PC12细胞的细胞活力和Bcl2水平降低,而使PC12细胞的凋亡指数和caspase 3水平增高; SP600125(5 μM)预处理不仅明显阻断LPA诱导的PC12细胞活力下降、细胞凋亡,并且极大地抑制了LPA诱导的JNK通路的激活、Bcl2水平的下调和caspase 3水平的上调。结论 JNK特异性抑制剂SP600125预处理能够明显阻断LPA诱导的PC12细胞损伤。
Abstract:
ObjectiveTo investigate the mechanisim of lysophosphatidic acid induced apoptosis of PC12 cells and suggest effective interventions.Methods The first experiment:PC12 cells were treated with various concentration of LPA(0、10、20、40 μM)for 24 hours,the second experiment: PC12 cells were treated with LPA(40 μM)for various time(0、6、12、24 h),the third experiment:normal group(0 μM LPA),experimental group(40 μM)and intervention group(pretreatment with 5 μM SP600125 for 2 hours+40 μM LPA)were cultured for 24 h. CCK-8 was used to determine the cell viability of PC12 cells. TUNEL staning was used to detect the apoptotic parameter of PC12 cells. Western Blot was used to investigate the expression/level of Bcl2,caspase 3 and phospho JNK in PC12 cells.Results LPA decreased the cell viability and Bcl2 expession level of PC12 cells while increased the apoptotic parameter and caspase 3 expression level of PC12 cells in a concentration-dependent/time-dependent manner. SP600125 preteatment not only significantly blocked LPA induced apoptosis and decreased the cell viability of PC12 cells,but also prevented LPA induced activation of JNK pathway,downregulation of Bcl2 and upregulation of caspase 3.Conclusion The preteatment with sp600125 was the specific inhibtor of JNK,could remarkably block LPA induced damage on PC12 cells.

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备注/Memo

备注/Memo:
基金项目:国家自然科学基金项目(No.81671051)
更新日期/Last Update: 2019-06-25