中国糖尿病杂志
中國糖尿病雜誌
중국당뇨병잡지
CHINESE JOURNAL OF DIABETES
2008年
6期
349-351
,共3页
孙子林%杨益宁%扬涛%马婵娟%刘必成%戴德哉%刘乃丰
孫子林%楊益寧%颺濤%馬嬋娟%劉必成%戴德哉%劉迺豐
손자림%양익저%양도%마선연%류필성%대덕재%류내봉
基质金属蛋白酶2%人肾系膜细胞%糖基化终产物%糖尿病肾病%氨基胍
基質金屬蛋白酶2%人腎繫膜細胞%糖基化終產物%糖尿病腎病%氨基胍
기질금속단백매2%인신계막세포%당기화종산물%당뇨병신병%안기고
Matrix metalloproteinase-2%Human renal mesangial cells% Advanced glycosylation end products% Aminoguanidine% Diabetic nephropathy
目的 观察盐酸氨基胍(AG)对糖基化终产物(AGEs)干预后人肾系膜细胞(HRMC)基质金属蛋白酶2(MMP-2)表达的影响. 方法运用糖基化终产物一牛血清白蛋白(AGE-BSA)干预HRMC,以及不同浓度AG单独或与AGE-BSA共同干预HRMC 24小时;RT-PCR和Western blot分别检测HRMC MMP-2 mRNA和蛋白表达. 结果 AGE-BSA明显降低HRMC MMP-2 mRNA和蛋白表达(P<0.05),AG以浓度依赖的方式恢复AGE-BSA下调的HRMC MMP-2 mRNA和蛋白表达(P<0.05). 结论 AG可能通过拮抗AGEs对MMP-2表达的抑制效应而发挥其肾脏保护作用.
目的 觀察鹽痠氨基胍(AG)對糖基化終產物(AGEs)榦預後人腎繫膜細胞(HRMC)基質金屬蛋白酶2(MMP-2)錶達的影響. 方法運用糖基化終產物一牛血清白蛋白(AGE-BSA)榦預HRMC,以及不同濃度AG單獨或與AGE-BSA共同榦預HRMC 24小時;RT-PCR和Western blot分彆檢測HRMC MMP-2 mRNA和蛋白錶達. 結果 AGE-BSA明顯降低HRMC MMP-2 mRNA和蛋白錶達(P<0.05),AG以濃度依賴的方式恢複AGE-BSA下調的HRMC MMP-2 mRNA和蛋白錶達(P<0.05). 結論 AG可能通過拮抗AGEs對MMP-2錶達的抑製效應而髮揮其腎髒保護作用.
목적 관찰염산안기고(AG)대당기화종산물(AGEs)간예후인신계막세포(HRMC)기질금속단백매2(MMP-2)표체적영향. 방법운용당기화종산물일우혈청백단백(AGE-BSA)간예HRMC,이급불동농도AG단독혹여AGE-BSA공동간예HRMC 24소시;RT-PCR화Western blot분별검측HRMC MMP-2 mRNA화단백표체. 결과 AGE-BSA명현강저HRMC MMP-2 mRNA화단백표체(P<0.05),AG이농도의뢰적방식회복AGE-BSA하조적HRMC MMP-2 mRNA화단백표체(P<0.05). 결론 AG가능통과길항AGEs대MMP-2표체적억제효응이발휘기신장보호작용.
Objective To investigate the effect of aminoguanidine(AG)on the matrix metalloproteinase-2(MMP-2)expression in advanced glycosylation end products(AGEs)-treated human renal mesangial cells(HRMC).Methods HRMCs were incubated with different concentrations of AG with or without AGE-BSA for 24 hours.The mRNA and protein expressions of MMP-2 in HRMC were analyzed by RT-PCR and Western blot,respectively.Results The expression levels of MMP-2 mRNA and protein in HRMC treated with AGE-BSA was significantly lower than that of control group(P<0.05).The depressed expressions of MMP-2 mRNA and protein in AGE-BSA-treated HRMC were increased by exposure to AG(P<0.05).Conclusions AG might play its reno-protection role via attenuation of AGEs-induced down-regulation of MMP-2