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. 2015 Jan;44(1):30-6.
doi: 10.3785/j.issn.1008-9292.2015.01.005.

[Neuroprotective effects of paeonol in a cell model of Parkinson disease]

[Article in Chinese]
Hao Wang  1 , Zhao-Ming Geng  2 , Zhi-Wei Hu  1 , Shu-Yan Wang  3 , Bing Zhao  3
Affiliations

[Neuroprotective effects of paeonol in a cell model of Parkinson disease]

[Article in Chinese]
Hao Wang et al. Zhejiang Da Xue Xue Bao Yi Xue Ban. 2015 Jan.

Abstract
in English, Chinese

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 PC12 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.

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、1 μmol/L丹皮酚组、3 μmol/L丹皮酚组和9 μmol/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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References

    1. SCHAPIRA A H, JENNER P. Etiology and pathogenesis of Parkinson's disease. Mov Disord. 2011;26(6):1049–1055. doi: 10.1002/mds.23732. - DOI - PubMed
    1. PERIER C, BOVE J, VILA M. Mitochondria and programmed cell death in Parkinson's disease: apoptosis and beyond. Antioxid Redox Signal. 2012;116(9):883–895. - PubMed
    1. BISAGLIA M, FILOGRANA R, BELTRAMINI M, et al. Are dopamine derivatives implicated in the pathogenesis of Parkinson's disease? Ageing Res Rev. 2014;13:107–114. doi: 10.1016/j.arr.2013.12.009. - DOI - PubMed
    1. ESPOSITO E, CUZZOCREA S. New therapeutic strategy for Parkinson's and Alzheimer's disease. Curr Med Chem. 2010;17(25):2764–2774. doi: 10.2174/092986710791859324. - DOI - PubMed
    1. 王 浩, 石 巧娟, 史 文珍, et al. 半胱氨酰白三烯受体CysLT_1R和CysLT_2R以及GPR17在帕金森病模型小鼠脑内的表达分布. http://www.cnki.com.cn/Article/CJFDTOTAL-ZJYB201301013.htm 浙江大学学报(医学版) 2013;42(1):52–60.