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作 者:宋志明[1] 王敏[1] 刘勇[1] 郝宝顺[1] 牛海名[1] 刘定辉[1] 余舒杰[1] 周彬[1] 吴琳[1] 余显冠 凌叶盛 彭沛[1] 朱洁明[1] 陈璘[1] 钱孝贤[1,2]
机构地区:[1]中山大学附属第三医院心血管内科,广东广州510630 [2]中西医结合研究所,广东广州510630
出 处:《中国病理生理杂志》2014年第8期1345-1350,共6页Chinese Journal of Pathophysiology
基 金:国家自然科学基金资助项目(No.81370447);广东省科技计划(No.2011B031800024;No.2011B031800155)
摘 要: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。AIM: To explore the effect of hydrogen sulfide on the senescence of human umbilical vein endothe -lial cells (HUVECs) induced by high glucose.METHODS: Senescence model was established by treating HUVECs with33 mmol/L glucose for 48 h.The parameters were detected to demonstrate the effect of hydrogen sulfide on senescence andthe mechanism involved was also investigated .RESULTS: In the cells treated with high glucose, the proliferation was attenuatedwith a higher number of senescence -associated β-galactosidase (SA-β-Gal) positive cells, and plasminogen activatorinhibitor 1 (PAI-1) protein expression, malondialdehyde (MDA) production and NF-κB p65 activity were increasedsignificantly, but the expression of superoxide dismutase 1 (SOD1) was decreased.However, the cell number and SOD1expression were increased, and the number of SA-β-Gal positive cells, PAI-1 protein expression, MDA production and theactivity of NF-κB p65 were decreased after sodium hydrosulfide (100 and 200 μmol/L) treatment.CONCLUSION: Exogenoushydrogen sulfide prevents HUVECs against high glucose -induced senescence by suppressing oxidative stress and NF -κB p65 activity.
关 键 词:硫化氢 内皮细胞 氧化性应激 NF-κB P65 高糖
分 类 号:R339.38[医药卫生—人体生理学]
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