摘要
目的观察氨基胍(AG)对体外制备的糖基化终产物(AGEs)诱导的人肾系膜细胞(HRMC)趋化因子fractalkine表达的影响。方法分别给予无血清的DMEM培养基、牛血清清蛋白(BSA)、糖基化终产物-牛血清清蛋白(AGE-BSA)干预HRMC,以及不同浓度AG与AGE-BSA共同干预HRMC 24 h;采用RT-PCR和Western-blot法分别检测HRMC fractalkine mRNA和蛋白表达。结果与DMEM、BSA组相比,AGE-BSA明显升高HRMC frac-talkine mRNA和蛋白表达(P<0.05),AG以浓度依赖的方式下调HRMC fractalkine mRNA和蛋白表达(P<0.05)。结论 AG可能通过拮抗AGEs对fractalkine表达的增加作用而发挥其肾脏保护作用。
Objective To investigate the effect of aminoguanidine （AG） on fractalkine expression of advanced glyeo- sylation end products （AGEs） treated human renal mesangial cells （HRMC） . Methods HRMC were incubated with DMEM, bovine serum albumin （BSA） and AGE - BSA respectively, as well as the combination of different concentrations of AG and AGE - BSA for 24 hours. The mRNA and protein expressions of fractalkine in HRMC were tested by RT - PCR and Westernblot respec- tively. Results The expression levels of fractalkine mRNA and protein in HRMC treated with AGE - BSA were significantly high- er than those in HRMC treated with DMEM and BSA （ P 〈 0. 05 ） . The down - regulation of mRNA and protein in HRMC by AG was concentration dependent （P 〈 0. 05 ） . Conclusion AG might play its renal protection role via the attenuation of the up - regulation of fraetalkine by AGEs.
出处
《中国全科医学》
CAS
CSCD
北大核心
2012年第27期3146-3148,共3页
Chinese General Practice
