丹皮酚抑制帕金森病模型细胞凋亡的作用
目的：观察丹皮酚对帕金森病模型细胞凋亡的影响。方法：采用1－甲基－4－苯基吡啶（ MPP＋）处理具有多巴胺能神经元特性的PC12细胞建立帕金森病体外模型，并分为正常对照组、空白对照组、1μmol／L丹皮酚组、3μmol／L丹皮酚组和9μmol／L丹皮酚组。以四甲基偶氮唑蓝比色法和乳酸脱氢酶法检测细胞损伤，以赫斯特荧光染剂染色及流式细胞术检测细胞凋亡，以二氯二氢荧光素－乙酰乙酸酯法检测细胞活性氧生成，以蛋白质印迹法检测凋亡相关蛋白半胱氨酸天冬氨酸蛋白酶－3（caspase－3）、Bcl－2和Bcl－2相关X蛋白（Bax）的表达水平。结果：与正常对照组比较，空白对照组细胞存活率显著降低，乳酸脱氢酶...
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| Published in | 浙江大学学报（医学版） no. 1; pp. 30 - 36 |
|---|---|
| Main Author | |
| Format | Journal Article |
| Language | Chinese |
| Published |
浙江省立同德医院神经内科,浙江杭州,310012%潍坊医学院临床医学系,山东潍坊,261053%浙江大学医学院附属第一医院麻醉科,浙江杭州,310003
2015
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1008-9292 |
| DOI | 10.3785/j.issn.1008-9292.2015.01.005 |
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| Abstract | 目的：观察丹皮酚对帕金森病模型细胞凋亡的影响。方法：采用1－甲基－4－苯基吡啶（ MPP＋）处理具有多巴胺能神经元特性的PC12细胞建立帕金森病体外模型，并分为正常对照组、空白对照组、1μmol／L丹皮酚组、3μmol／L丹皮酚组和9μmol／L丹皮酚组。以四甲基偶氮唑蓝比色法和乳酸脱氢酶法检测细胞损伤，以赫斯特荧光染剂染色及流式细胞术检测细胞凋亡，以二氯二氢荧光素－乙酰乙酸酯法检测细胞活性氧生成，以蛋白质印迹法检测凋亡相关蛋白半胱氨酸天冬氨酸蛋白酶－3（caspase－3）、Bcl－2和Bcl－2相关X蛋白（Bax）的表达水平。结果：与正常对照组比较，空白对照组细胞存活率显著降低，乳酸脱氢酶漏出率升高，凋亡细胞增多，活性氧生成增加，凋亡相关分子caspase－3活性上调、Bax／Bcl－2比值升高，差异均具有统计学意义（均P＜0．01）。与空白对照组比较，各浓度丹皮酚预处理后细胞存活率显著升高，乳酸脱氢酶漏出率降低，凋亡细胞减少，并抑制活性氧生成，降低Bax／Bcl－2的比值及caspase－3蛋白水平，差异均具有统计学意义（ P＜0．05或P＜0．01）。结论：丹皮酚能抑制帕金森病模型PC12细胞凋亡，其发挥保护作用的机制可能与改善氧化应激、降低Bax／Bcl－2比值、抑制caspase－3活化有关。 |
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| AbstractList | R96; 目的：观察丹皮酚对帕金森病模型细胞凋亡的影响。方法：采用1－甲基－4－苯基吡啶（ MPP＋）处理具有多巴胺能神经元特性的PC12细胞建立帕金森病体外模型，并分为正常对照组、空白对照组、1μmol／L丹皮酚组、3μmol／L丹皮酚组和9μmol／L丹皮酚组。以四甲基偶氮唑蓝比色法和乳酸脱氢酶法检测细胞损伤，以赫斯特荧光染剂染色及流式细胞术检测细胞凋亡，以二氯二氢荧光素－乙酰乙酸酯法检测细胞活性氧生成，以蛋白质印迹法检测凋亡相关蛋白半胱氨酸天冬氨酸蛋白酶－3（caspase－3）、Bcl－2和Bcl－2相关X蛋白（Bax）的表达水平。结果：与正常对照组比较，空白对照组细胞存活率显著降低，乳酸脱氢酶漏出率升高，凋亡细胞增多，活性氧生成增加，凋亡相关分子caspase－3活性上调、Bax／Bcl－2比值升高，差异均具有统计学意义（均P＜0．01）。与空白对照组比较，各浓度丹皮酚预处理后细胞存活率显著升高，乳酸脱氢酶漏出率降低，凋亡细胞减少，并抑制活性氧生成，降低Bax／Bcl－2的比值及caspase－3蛋白水平，差异均具有统计学意义（ P＜0．05或P＜0．01）。结论：丹皮酚能抑制帕金森病模型PC12细胞凋亡，其发挥保护作用的机制可能与改善氧化应激、降低Bax／Bcl－2比值、抑制caspase－3活化有关。 目的：观察丹皮酚对帕金森病模型细胞凋亡的影响。方法：采用1－甲基－4－苯基吡啶（ MPP＋）处理具有多巴胺能神经元特性的PC12细胞建立帕金森病体外模型，并分为正常对照组、空白对照组、1μmol／L丹皮酚组、3μmol／L丹皮酚组和9μmol／L丹皮酚组。以四甲基偶氮唑蓝比色法和乳酸脱氢酶法检测细胞损伤，以赫斯特荧光染剂染色及流式细胞术检测细胞凋亡，以二氯二氢荧光素－乙酰乙酸酯法检测细胞活性氧生成，以蛋白质印迹法检测凋亡相关蛋白半胱氨酸天冬氨酸蛋白酶－3（caspase－3）、Bcl－2和Bcl－2相关X蛋白（Bax）的表达水平。结果：与正常对照组比较，空白对照组细胞存活率显著降低，乳酸脱氢酶漏出率升高，凋亡细胞增多，活性氧生成增加，凋亡相关分子caspase－3活性上调、Bax／Bcl－2比值升高，差异均具有统计学意义（均P＜0．01）。与空白对照组比较，各浓度丹皮酚预处理后细胞存活率显著升高，乳酸脱氢酶漏出率降低，凋亡细胞减少，并抑制活性氧生成，降低Bax／Bcl－2的比值及caspase－3蛋白水平，差异均具有统计学意义（ P＜0．05或P＜0．01）。结论：丹皮酚能抑制帕金森病模型PC12细胞凋亡，其发挥保护作用的机制可能与改善氧化应激、降低Bax／Bcl－2比值、抑制caspase－3活化有关。 |
| Abstract_FL | Objective:To investigate the effects of paeonol on neuron cell model of Parkinson disease ( PD) .Methods: The cell model of Parkinson disease was induced by treatment of 1-Methyl-4-phenylpyridinium ( MPP+) in PC12 cells, the PD model cells were treated with 1 μmol/L, 3 μmol/L or 9 μmol/L paeonol for 24h, respectively.Cell viability and LDH leakage were detected by MTT and lactate dehydrogenase ( LDH) assay; the apoptosis of PC12 cells was assessed by Hoechst 33258 staining and flow cytometry; reactive oxygen species ( ROS ) production was detected by DCFH-DA method;and the ratio of Bax/Bcl-2 and activation of caspase-3 were determined by Western blotting .Results: MPP+treatment significantly reduced cell viability , increased LDH leakage , enhanced the proportion of apoptotic cells and ROS production .In addition , MPP+ treatment dramatically increased the Bax/Bcl-2 ratio, and the activation of caspase-3.Compared to PD model group , paeonol treatment significantly enhanced cell viability , decreased LDH leakage , inhibited the proportion of apoptotic cells and ROS production , reduced the Bax/Bcl-2 ratio and the activated caspase-3 protein .Conclusion:Paeonol can prevent PC 12 cells from apoptosis induced by MPP+, and the mechanism may be associated with the down-regulation of ROS production, Bax/Bcl-2 ratio and Caspase-3 activation. |
| Author | 王浩 耿赵铭 胡智伟 王舒燕 赵冰 |
| AuthorAffiliation | 浙江省立同德医院神经内科,浙江杭州310012 潍坊医学院临床医学系,山东潍坊261053 浙江大学医学院附属第一医院麻醉科,浙江杭州310003 |
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| Author_FL | GENG Zhao-ming WANG Shu-yan HU Zhi-wei WANG Hao ZHAO Bing |
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| DOI | 10.3785/j.issn.1008-9292.2015.01.005 |
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| DocumentTitleAlternate | Neuroprotective effects of paeonol in a cell model of Parkinson disease |
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| Keywords | Paeonol/administration & dosage Reactive oxygen species 帕金森病 bcl-2-associated X protein 牡丹酚/投药和剂量 半胱氨酸天冬氨酸蛋白酶3/药物作用 Paeonol/pharmacology Caspase 3/drug effects 1-甲基-4-苯基吡啶 Parkinsondisease bcl-2相关X蛋白质 1-Methyl-4-phenylpyridinium 细胞凋亡/药物作用 Genes,bcl-2 牡丹酚/药理学 活性氧 Apoptosis/drug effect 基因, bcl-2 |
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| Notes | 33-1248/R Objective：To investigate the effects of paeonol on neuron cell model of Parkinson disease （ PD） .Methods： The cell model of Parkinson disease was induced by treatment of 1-Methyl-4-phenylpyridinium （ MPP＋） in PC12 cells, the PD model cells were treated with 1 μmol/L, 3 μmol/L or 9 μmol/L paeonol for 24h, respectively.Cell viability and LDH leakage were detected by MTT and lactate dehydrogenase （ LDH） assay; the apoptosis of PC12 cells was assessed by Hoechst 33258 staining and flow cytometry; reactive oxygen species （ ROS ） production was detected by DCFH-DA method;and the ratio of Bax/Bcl-2 and activation of caspase-3 were determined by Western blotting .Results： MPP＋treatment significantly reduced cell viability , increased LDH leakage , enhanced the proportion of apoptotic cells and ROS production .In addition , MPP＋ treatment dramatically increased the Bax/Bcl-2 ratio, and the activation of caspase-3.Compared to PD model group , paeonol treatment significantly enhanced cell viability , decreased |
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| Publisher | 浙江省立同德医院神经内科,浙江杭州,310012%潍坊医学院临床医学系,山东潍坊,261053%浙江大学医学院附属第一医院麻醉科,浙江杭州,310003 |
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| Snippet | 目的：观察丹皮酚对帕金森病模型细胞凋亡的影响。方法：采用1－甲基－4－苯基吡啶（ MPP＋）处理具有多巴胺能神经元特性的PC12细胞建立帕金森病体外模型，并分为正常对照... R96; 目的：观察丹皮酚对帕金森病模型细胞凋亡的影响。方法：采用1－甲基－4－苯基吡啶（ MPP＋）处理具有多巴胺能神经元特性的PC12细胞建立帕金森病体外模型，并分为正常... |
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| SubjectTerms | 1-甲基-4-苯基吡啶 bcl-2 bcl-2相关X蛋白质 半胱氨酸天冬氨酸蛋白酶3/药物作用 基因 帕金森病 活性氧 牡丹酚/投药和剂量 牡丹酚/药理学 细胞凋亡/药物作用 |
| Title | 丹皮酚抑制帕金森病模型细胞凋亡的作用 |
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