Hydrogen sulfide protects SH-SY5Y neuronal cells against D-galactose induced cell injury by suppression of advanced glycation end products formation and oxidative stress
Hydrogen sulfide protects SH-SY5Y neuronal cells against D-galactose induced cell injury by suppression of advanced glycation end products formation and oxidative stress
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DOI：
10.1016/j.neuint.2012.12.010
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发表时间：
2013-04-01
影响因子：
4.2
通讯作者：
Bian, Jin-Song
中科院分区：
文献类型：
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作者：
Liu, Yan-Ying;Nagpure, Bhushan Vijay;Bian, Jin-Song
D-半乳糖被广泛用作导致实验动物衰老的药物。本研究旨在探讨硫化氢 (H2S) 对暴露于 D-半乳糖的人神经母细胞瘤 SH-SY5Y 细胞的影响。细胞用 NaHS（H2S 供体）预处理，然后暴露于 D-半乳糖（25-400 mM，48 小时）。我们发现 NaHS 预处理显着逆转了 D-半乳糖诱导的细胞死亡和细胞衰老。 MTT 测定显示，与 D-半乳糖 (200 mM) 处理组相比，NaHS 显着增加了细胞活力，从 62.31 +/- 1.29% 增加到 72.34 +/- 0.46%。其潜在机制似乎涉及 NaHS 减少晚期糖基化终末产物 (AGE) 的形成，而众所周知，晚期糖基化终产物 (AGE) 会导致与年龄相关的疾病的进展。此外，在 D-半乳糖暴露后，NaHS 使 SH-SY5Y 细胞中活性氧的升高从 151.17 +/- 2.07% 降低至 124.8 +/- 2.89%，丙二醛的升高从 1.72 +/- 0.07 降低至 1.10 +/- 0.08（nmol/mg 蛋白质）。 NaHS 还刺激超氧化物歧化酶的活性从 0.42 +/- 0.05 到 0.73 +/- 0.04（U/mg 蛋白质）和谷胱甘肽过氧化物酶从 3.98 +/- 0.73 到 14.73 +/- 0.77（nmol/min/mg 蛋白质），并上调铜转运蛋白 ATOX1、谷胱甘肽合成酶（GSS）和硫氧还蛋白还原酶 1 (TXNRD1)，同时下调醛氧化酶 1 (AOX1)。总之，我们的数据表明，H2S 可能通过抑制 AGE 形成和减少氧化应激而具有潜在的抗衰老作用。 (C) 2013 Elsevier Ltd. 保留所有权利。
D-Galactose is widely used as an agent to cause aging effects in experimental animals. The present study aims to investigate the effects of hydrogen sulfide (H2S) in human neuroblastoma SH-SY5Y cells exposed to D-galactose. Cells were pretreated with NaHS, an H2S donor, and then exposed to D-galactose (25-400 mM for 48 h). We found that NaHS pretreatment significantly reversed the D-galactose-induced cell death and cellular senescence. MTT assay shows that NaHS significantly increased cell viability from 62.31 +/- 1.29% to 72.34 +/- 0.46% compared with D-galactose (200 mM) treatment group. The underlying mechanism appeared to involve a reduction by NaHS in the formation of advanced glycation end products (AGEs), which are known to contribute to the progression of age-related diseases. In addition, NaHS decreased the elevation of reactive oxygen species from 151.17 +/- 2.07% to 124.8 +/- 2.89% and malondialdehyde from 1.72 +/- 0.07 to 1.10 +/- 0.08 (nmol/mg protein) in SH-SY5Y cells after D-galactose exposure. NaHS also stimulated activities of superoxide dismutase from 0.42 +/- 0.05 to 0.73 +/- 0.04 (U/mg protein) and glutathione peroxidase from 3.98 +/- 0.73 to 14.73 +/- 0.77 (nmol/min/mg protein) and upregulated the gene expression levels of copper transport protein ATOX1, glutathione synthetase (GSS) and thioredoxin reductase 1 (TXNRD1) while down-regulated aldehyde oxidase 1 (AOX1). In summary, our data indicate that H2S may have potentially anti-aging effects through the inhibition of AGEs formation and reduction of oxidative stress. (C) 2013 Elsevier Ltd. All rights reserved.