Paeoniflorin exerts neuroprotective effects against glutamate‑induced PC12 cellular cytotoxicity by inhibiting apoptosis.
Paeoniflorin exerts neuroprotective effects against glutamate‑induced PC12 cellular cytotoxicity by inhibiting apoptosis.
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芍药苷通过抑制细胞凋亡对谷氨酸诱导的 PC12 细胞毒性发挥神经保护作用
DOI：
10.3892/ijmm.2017.3076
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发表时间：
2017-09
影响因子：
5.4
通讯作者：
Lin Y
中科院分区：
文献类型：
--
作者：
Chen A;Wang H;Zhang Y;Wang X;Yu L;Xu W;Xu W;Lin Y
芍药苷（PF）是中药芍药的有效成分，具有神经保护作用。然而，PF的神经保护作用背后的机制尚未完全了解。神经元凋亡在脑缺血诱导的级联反应中起重要作用。本研究旨在探讨PF对谷氨酸诱导的PC 12细胞毒性的神经保护作用，并确定这些作用是否通过抑制体外细胞凋亡和PC 12细胞线粒体凋亡相关蛋白的活性介导。暴露于谷氨酸诱导的PC 12细胞的细胞形态学变化，显着降低细胞活力和诱导凋亡，从Hoechst 33342染色和膜联蛋白V/PI染色实验观察到类似的结果。谷氨酸还增加了PC 12细胞的乳酸脱氢酶释放。然而，PF治疗可预防这些效应。此外，PF还抑制Bax和Bad的表达，增加Bcl-2和Bcl-xL的表达，并降低下游蛋白caspase-3和caspase-9的水平。总的来说，我们的研究结果表明，PF保护PC 12细胞对谷氨酸诱导的神经毒性可能通过抑制线粒体凋亡相关蛋白的表达。
Paeoniflorin (PF) is an active ingredient of Radix Paeoniae, which is known to exert neuroprotective effects. However, the mechanims behind the neuroprotective effects of PF are not yet fully understood. The apoptosis of neurons plays an important role in the cerebral ischemia-induced cascade response. This study aimed to investigate neuroprotective effects of PF against glutamate-induced PC12 cellular cytotoxicity and to determine whether these effects are mediated via the inhibition of apoptosis in vitro and the activity of mitochondrial apoptosis-associated proteins in PC12 cells. Exposure of the PC12 cells to glutamate induced cell morphological changes, significantly decreased cell viability and induced apoptosis, with similar results being observed from the Hoechst 33342 staining and Annexin V/PI staining experiments. Glutamate also increased the lactate dehydrogenase release by the PC12 cells. However, treatment with PF prevented these effects. Furthermore, PF inhibited Bax and Bad expression and increased Bcl-2 and Bcl-xL expression; it also decreased the levels of downstream protein (caspase-3 and caspase-9). Collectively, our results indicate that PF protects PC12 cells against glutamate-induced neurotoxicity possibly through the inhibition of the expression of mitochondrial apoptosis-associated proteins.
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影响因子：
3.4
作者：
Li, Huang;Ye, Miao;Que, Jinhua
通讯作者：
Que, Jinhua
影响因子：
4.2
作者：
Ouyang YB;Giffard RG
通讯作者：
Giffard RG
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4
作者：
Mao, Qing-Qiu;Zhong, Xiao-Ming;Huang, Zhen
通讯作者：
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影响因子：
1.7
作者：
Cao, Li-Li;Du, Guan-Hua;Wang, Min-Wei
通讯作者：
Wang, Min-Wei
影响因子：
5.4
作者：
Cao, Bi-Yin;Yang, Ya-Ping;Liu, Chun-Feng
通讯作者：
Liu, Chun-Feng