摘要
背景:脑缺血再灌注损伤(CIR)是缺血性脑卒中的主要病理机制,氧化应激(OS)在脑缺血再灌注过程中起着重要作用。近期研究E发现OS能激活MAPK通路,主要作为细胞应激的中介。这表明H2S可能具有多种生物学功能,通过保护神经保护作用。抗OS所致神经元损伤。但H2S如何通过MAPK信号通路减轻缺血/复氧损伤尚不清楚。外源硫化氢(H2S)对氧的保护机制本研究研究了SH-SY5Y细胞生理剂量下的GG剥夺/复氧(OGD/R)。 方法:用DCFH-DA探针检测细胞内ROS,实时PCR和Western blot检测p38MAPK、ERK 3和Nrf 2的表达。用CCK-8检测细胞活力。 结果:与正常对照组相比,其他3组在24h开始时ERK 3、p38MAPK和Nrf 2 mRNA表达下调。24h后,ERK 3,p38MAPK和Nrf 2较正常对照组显著升高。200μM nahs预处理细胞24h后,ERK 3、p38MAPK和Nrf 2的表达与OGD/R组和NAHS组相比,其下降更为显著。 结论:外源性H2S通过增强ERK 3、p38MAPK和Nrf 2 mRNA的激活,对OGD/R诱导的损伤有保护作用。
关键词: 硫化氢,缺氧-葡萄糖剥夺,复氧,ERK 3,p38MAPK,Nrf 2。
Current Molecular Medicine
Title:Exogenous Hydrogen Sulfide Protects SH-SY5Y Cells from OGD/RInduced Injury
Volume: 17 Issue: 8
关键词: 硫化氢,缺氧-葡萄糖剥夺,复氧,ERK 3,p38MAPK,Nrf 2。
摘要: Background: Cerebral ischemia reperfusion (CIR) injury is the main pathological mechanism of ischemia stroke, and oxidative stress (OS) plays a vital role during the process of CIR. Recent studies have found that OS can activate MAPK pathway, which mainly functions as a mediator of cellular stresses. It revealed that H2S may exhibit multiple biological functions as a neuroprotector through protecting against OS-induced neuronal injury. But how H2S can attenuate ischemia/reoxygenation injury through MAPK signaling is not clear. The protective mechanism of exogenous hydrogen sulfide (H2S) on oxygen glucose deprivation/reoxygenation (OGD/R) at physiological doses in SH-SY5Y cells were investigated in this study.
Methods: DCFH- DA probe is used to measure intracellular ROS, Real-time PCR and Western blot are used to detect the levels of p38 MAPK, ERK3 and Nrf2. CCK-8 is used to detect cell viability.
Results: Comparing with the normal control group, the expressions of ERK3, p38MAPK and Nrf2 mRNA in other three groups were downregulated at the beginning of 24h. After 24h, the expressions of ERK3, p38MAPK and Nrf2 were upregulated significantly compared with the normal control group. When the cells were pretreated with 200μM NaHS at the beginning of 24h, the expressions of ERK3, p38MAPK and Nrf2 were decreased much more significantly than OGD/R and NaHS groups.
Conclusion: The present study demonstrated that exogenous H2S exerts a protective effect against OGD/R-induced injury by enhancing the activation of the ERK3, p38MAPK and Nrf2 mRNA.
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Exogenous Hydrogen Sulfide Protects SH-SY5Y Cells from OGD/RInduced Injury, Current Molecular Medicine 2017; 17 (8) . https://dx.doi.org/10.2174/1566524018666180222121643
DOI https://dx.doi.org/10.2174/1566524018666180222121643 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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