硫化氢通过抑制氧化应激改善高糖诱导的内皮细胞衰老

目的:探讨外源性硫化氢对高糖诱导的人脐静脉内皮细胞(HUVECs)衰老的作用及机制。方法:建立高糖(33 mmol/L葡萄糖)诱导的HUVECs早熟型衰老模型,观察硫化氢对衰老的作用及其相关的分子机制。结果:HUVECs经高糖处理后,细胞生长缓慢,衰老相关β半乳糖苷酶染色(SA-β-Gal)阳性细胞数目增加,血浆纤溶酶原激活物抑制剂1(PAI-1)表达明显增高,超氧化物歧化酶1(SOD1)显著减少,丙二醛(MDA)产量明显增多,核因子κB p65(NF-κB p65)活性增加;与模型组比较,100μmol/L和200μmol/L硫氢化钠(硫化氢供体)处理组的细胞数目明显增加,SA-β-Gal染色阳性细胞数目及PAI-1蛋白表达显著下降,SOD1表达明显增加,MDA产量明显减少,NF-κB p65活性降低。结论:硫化氢能通过抑制氧化应激反应和NF-κB p65活性而抵抗高糖诱导的HUVECs衰老。

Hydrogen sulfide ameliorates high glucose-induced endothelial cell senescence by suppressing oxidative stress

AIM：To explore the effect of hydrogen sulfide on the senescence of human umbilical vein endothelial cells (HUVECs) induced by high glucose. METHODS：Senescence model was established by treating HUVECs with 33 mmol/L glucose for 48 h. The parameters were detected to demonstrate the effect of hydrogen sulfide on senescence and the mechanism involved was also investigated. RESULTS：In the cells treated with high glucose, the proliferation was attenuated with a higher number of senescence-associated β-galactosidase (SA-β-Gal) positive cells, and plasminogen activator inhibitor 1 (PAI-1) protein expression, malondialdehyde (MDA) production and NF-κB p65 activity were increased significantly, but the expression of superoxide dismutase 1 (SOD1) was decreased. However, the cell number and SOD1 expression were increased, and the number of SA-β-Gal positive cells, PAI-1 protein expression, MDA production and the activity of NF-κB p65 were decreased after sodium hydrosulfide (100 and 200 μmol/L) treatment.CONCLUSION：Exo-genous hydrogen sulfide prevents HUVECs against high glucose-induced senescence by suppressing oxidative stress and NF-κB p65 activity.