摘要
目的:研究α-硫辛酸对高糖毒性作用后βTc6细胞胰岛素基因、肌腱膜纤维肉瘤癌基因同系物A(MafA)基因表达的影响,对细胞的保护作用及其机制。方法:培养βTc6细胞,分为NG组(5mmol/L葡萄糖)、HG组(16.7mmol/L葡萄糖)和HG+ALA组(16.7mmol/L葡萄糖+200μmol/Lα-硫辛酸);培养48h后收集细胞培养液,检测胰岛素浓度并提取细胞总RNA,逆转录-聚合酶链反应检测胰岛素及MafAmRNA水平。结果:HG组与NG组比较,胰岛素和MafAmRNA的表达下降(P<0.05或P<0.01);HG+ALA组与HG组相比,胰岛素和MafAmRNA的表达均提高(均P<0.01);而与NG组相比,胰岛素和MafAmRNA的表达差异均无统计学意义(均P>0.05)。结论:糖毒性可能通过激活βTc6细胞内氧化应激反应使MafA的表达下降,进而导致胰岛素基因表达下降;α-硫辛酸可能通过上调MafA的表达而对β细胞起到保护作用。
Objective：To study the impact of elevated glucose on the expression of insulin gene and insulin transcript factor v-maf musculoaponeurotic fibrosarcoma oncogene homologue A（MafA） gene,and to clarify the mechanism of the protection of α-lipoic acid for β cell under oxidative stress.Methods：βTc6 cells were cultured in DMEM,and then cultured for 48 h in media containing 5 mmol/L glucose（NG group）,16.7 mmol/L glucose（HG group） and 16.7 mmol/L glucose and 200 μmol/L α-lipoic acid（HG＋ALA group） respectively.The insulin concentration in supernatant of cells cultured in different glucose medium was assayed by RNA after 48 h culture period.The mRNA expression levels of insulin and MafA were determined by RT-PCR.Results：In HG group,insulin mRNA level（P 〈 0.05） and MafA mRNA level（P 〈 0.01） were decreased compared with those of NG group.The insulin mRNA level（P 〈 0.01） and MafA mRNA level（P 〈 0.01） were increased in HG＋ALA group than those of HG group.There was no significant difference in insulin and MafA mRNA levels between NG group and HG ＋ ALA group（P 〉 0.05）.Conclusion：These data suggested that elevated glucose concentrations led to a decrease in insulin and insulin transcript factor MafA mRNA levels in βTc6 cells.α-lipoic acid could attenuate this impact of elevated glucose through increasing the expression level of MafA.
出处
《天津医药》
CAS
北大核心
2011年第7期612-614,共3页
Tianjin Medical Journal
关键词
糖尿病
2型
胰岛素
氧化性应激
硫辛酸
RNA
信使
胰岛素分泌细胞
血糖
肌腱膜纤维肉瘤
癌基因同系物
diabetes mellitus； type 2 insulin oxidative stress thioctic acid RNA； messenger insulin-secreting cells blood glucose v-maf musculoaponeurotic fibrosarcoma oncogene homologue A
