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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Protection of capsaicin against hypoxia-reoxygenation-induced apoptosis of rat hippocampal neurons.
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Protection of capsaicin against hypoxia-reoxygenation-induced apoptosis of rat hippocampal neurons.

机译：辣椒素对缺氧-复氧诱导的大鼠海马神经元凋亡的保护作用。

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摘要

The aim of this study was to investigate the effect of capsaicin on hypoxia-reoxygenation (H/R)-induced apoptosis in primary rat hippocampal neurons. Three hours of hypoxia (1% O2) and subsequent reoxygenation for 24 h significantly increased the apoptotic death of hippocampal neurons, as evidenced by increases in both TUNEL-positive cell number and caspase-3 activity. Pretreatment with capsaicin (3-30 micromol/L) or the caspase-3-specific inhibitor acetyl-DEVD-CHO (100 micromol/L) markedly attenuated H/R-induced apoptosis in hippocampal neurons. Capsaicin also markedly induced the phosphorylation of Akt. The phosphoinositide 3-kinase (PI3K) inhibitor LY294002 (10 micromol/L) prevented any capsaicin-induced survival effect in hippocampal neurons. Intracellular levels of reactive oxygen species (ROS), which were greatly increased after H/R, were significantly inhibited by capsaicin, pyrrolidine dithiocarbamate (PDTC) (50 micromol/L), and LY294002. Taken together, these data suggest that capsaicin protects against H/R-induced apoptosis of hippocampal neurons via the PI3K/Akt-mediated signaling pathway, which is related to the inhibition of oxidative stress and caspase-3 activation.
机译：这项研究的目的是调查辣椒素对缺氧-复氧（H / R）诱导的原代大鼠海马神经元凋亡的影响。 3小时的缺氧（1％O2）和随后的复氧24 h明显增加了海马神经元的凋亡死亡，这由TUNEL阳性细胞数量和caspase-3活性的增加所证明。辣椒素（3-30 micromol / L）或半胱天冬酶3特异性抑制剂乙酰基-DEVD-CHO（100 micromol / L）预处理显着减弱了H / R诱导的海马神经元凋亡。辣椒素还显着诱导Akt的磷酸化。磷酸肌醇3-激酶（PI3K）抑制剂LY294002（10 micromol / L）阻止了辣椒素诱导的海马神经元存活效应。辣椒素，吡咯烷二硫代氨基甲酸酯（PDTC）（50 micromol / L）和LY294002显着抑制了H / R后细胞内活性氧（ROS）的水平显着增加。综上所述，这些数据表明辣椒素可通过PI3K / Akt介导的信号通路防止H / R诱导的海马神经元凋亡，这与抑制氧化应激和caspase-3活化有关。

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