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首页> 外文期刊>Journal of drug targeting >Stomatin-like protein-2 confers neuroprotection effect in oxygen-glucose deprivation/reoxygenation-injured neurons by regulating AMPK/Nrf2 signalling
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Stomatin-like protein-2 confers neuroprotection effect in oxygen-glucose deprivation/reoxygenation-injured neurons by regulating AMPK/Nrf2 signalling

机译：STOPTIN样蛋白-2通过调节AMPK / NRF2信号传导来赋予氧葡萄糖剥夺/雷诺损伤的神经元中的神经保护作用

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摘要

Stomatin-like protein-2 (SLP-2) has emerged as a cytoprotective protein that confers a protective effect against various stresses. However, whether SLP-2 confers neuroprotection during cerebral ischemia/reperfusion injury remains unclear. In the present study, we investigated the role of SLP-2 in regulating oxygen-glucose deprivation/reoxygenation (OGD/R)-induced apoptosis and oxidative stress, which has been used as an in vitro model of cerebral ischemia/reperfusion injury. We found that OGD/R treatment resulted in a significant reduction in SLP-2 expression in neurons. Functional experiments demonstrated that SLP-2 overexpression significantly increased cell viability and decreased cell apoptosis and reactive oxygen species (ROS) production in OGD/R-exposed neurons, while SLP-2 inhibition showed the opposite effect. Notably, SLP-2 overexpression was shown to up-regulate the phosphorylation of adenosine monophosphate-activated protein kinase (AMPK). In addition, SLP-2 overexpression increased the nuclear expression of nuclear factor (erythroid-derived 2)-like 2 and reinforced the activity of Nrf2/antioxidant response element (ARE)-mediated transcription. However, AMPK inhibition or Nrf2/ARE inhibition partially reversed SLP-2-mediated neuroprotection effect in OGD/R-exposed neurons. Taken together, these results demonstrate that SLP-2 confers neuroprotection effect in OGD/R-injured neurons associated with reinforcing AMPK/Nrf2 signalling, suggesting SLP-2 as a potential therapeutic target for cerebral ischemia/reperfusion injury.
机译：气孔素样蛋白-2（SLP-2）是一种细胞保护蛋白，对各种应激具有保护作用。然而，SLP-2在脑缺血/再灌注损伤中是否具有神经保护作用尚不清楚。在本研究中，我们研究了SLP-2在调节氧-糖剥夺/复氧（OGD/R）诱导的细胞凋亡和氧化应激中的作用，这已被用作脑缺血/再灌注损伤的体外模型。我们发现OGD/R治疗可显著降低神经元中SLP-2的表达。功能实验表明，在OGD/R暴露的神经元中，SLP-2的过度表达显著增加了细胞活力，减少了细胞凋亡和活性氧（ROS）的产生，而SLP-2的抑制则表现出相反的效果。值得注意的是，SLP-2过度表达可上调单磷酸腺苷活化蛋白激酶（AMPK）的磷酸化。此外，SLP-2过表达增加了核因子（红系衍生2）样2的核表达，并增强了Nrf2/抗氧化反应元件（ARE）介导的转录活性。然而，AMPK抑制或Nrf2/ARE抑制部分逆转了在OGD/R暴露的神经元中SLP-2介导的神经保护作用。总之，这些结果表明，SLP-2对OGD/R损伤的神经元具有神经保护作用，与增强AMPK/Nrf2信号有关，表明SLP-2是脑缺血/再灌注损伤的潜在治疗靶点。

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