晚期糖基化终产物对人肾小管上皮细胞增殖和凋亡的影响  

Effects of advanced glycation end products on proliferation and apotosis of human renal tubular epithelial cells

作　　者：李琳娜[1] 王利娟[1] 何可可[2] 李海成[1] 何金花[1] 蒋建伟[1] 刘誉[1] 

机构地区：[1]暨南大学医学院生物化学教研室,广东广州510632 [2]中山大学第三附属医院放射科,广东广州510630

出　　处：《暨南大学学报（自然科学与医学版）》2008年第2期125-129,共5页Journal of Jinan University(Natural Science & Medicine Edition)

基　　金：暨南大学引进人才启动基金资助项目(51204004);广州市科技计划资助项目(2002J1-C0361)

摘　　要：目的:研究晚期糖基化终产物(advanced glycation end products,AGEs)对人肾小管上皮细胞株(HKC)的细胞毒性作用。方法:以体外培养的HKC细胞为研究对象,采用MTT法测定不同质量浓度(0、50、100、200、400、800 mg/L)AGEs对HKC生长的抑制作用,应用流式细胞仪分析细胞的凋亡情况,RT-PCR分析不同浓度AGEs处理HKC后其IL-1β,TNF-α,HMGB1基因的转录水平变化。结果:AGEs质量浓度为100、200、400、800 mg/L时分别刺激HKC细胞24和48 h后,均能显著抑制细胞的增殖,且抑制作用具有时间和剂量依赖性。流式细胞仪分析发现,AGEs能促使HKC发生凋亡,凋亡率亦随AGEs浓度的增高而增加。RT-PCR方法检测显示,AGEs使HKC细胞IL-1β、TNF-α、HMGB1基因的表达上调。结论:AGEs可抑制人肾小管上皮细胞的增殖,并诱导其发生凋亡,此作用可能与其上调IL-1β、TNF-α和HMGB1基因的表达有关。Aim：To investigate the cytotoxicity of human renal tubular epithelial cells（HKC） induced by advanced glycation end products（AGEs）. Methods： The proliferative inhibition of HKC by AGEs at different concentrations （0,50,100,200,400,800 mg/L） was accessed by using MTF assay. Cell apoptosis was analyzed by flow cytometry. The mRNA levels of IL-1β, TNF-α and HMGB1 were determined by RT-PCR. Results： AGEs at 100,200,400,800 mg/L significantly inhibited proliferation of HKC after incubation with AGEs for 24 and 48 h, which showed good time-and dose-dependent fashions. AGEs were also found to cause apoptosis in HKC. The flow cytometry analysis showed that AGEs increased the proportion of apoptotic cells in a dose-dependent manner, while RT-PCR analysis demonstrated that the mRNA expression levels of IL-1β, TNF-αand HMGB1 in HKC cells were up-regulated by AGEs. Conclusion：AGEs can inhibit proliferation and also induce apoptosis in HKC. These effects may be related to the up-regulated expression of IL-1β, TNF-α and HMGB1 genes.

关 键 词：晚期糖基化终产物 细胞毒性 人肾小管上皮细胞 

分 类 号：R318.16[医药卫生—生物医学工程]