中国药理学通报2017，Vol.33Issue(3)：348-353,6.DOI:10.3969/j.issn.1001-1978.2017.03.012
胰高血糖素样肽-1对AGEs诱导H9 C2心肌细胞自噬的影响
The protective effect of glucogon like peptide-1 on H9 C2 cardimyocytes against AGEs-induced injury by inhibiting excessive autophagy
摘要
Abstract
Aim Toinvestigatetheeffectofglucogon like peptide-1 on H9 C2 cardiomyocytes against AGEs-induced injury and potential protective mechanisms of autophagy.Methods CulturedH9C2cardiomyocytes were respectively incubated with 0. 9% NaCl,100 mg ·L-1 AGEs,100 mg · L-1 AGEs +10 nmol · L-1 GLP-1 ,100 mg·L-1 AGEs+10 nmol·L-1 GLP-1 +5μmol·L-1 rapamycinfor 24 h.Intracellular ROS pro-duction was measured by DCFH-DA fluorescent probe. Cell viability was quantified by CCK-8 assay.Nucleus morphology was observed under fluorescence micro-scope after being incubated with Honchest 33258.The formations of autolysosomes were detected by flow cy-tometry using the PH-sensitive fluorescent dye acridine orange(OA).Western blot was applied to assess theexpression of autophagy-associated protein including LC3Ⅱ,Beclin-1.Results AGEsimpairedcellviabil-ity,increased intracellular ROS production,enhanced formation of autolysosomes and up-regulated expression of LC3Ⅱand Beclin-1;however,the effect were re-versed remarkably by GLP-1 .Furthermore,effect of GLP-1 was inhibited by rapamycin(autophagy agonist) in cell viability,amount of autolysosomes,and expres-sion of autophagy-associated protein but not in intracel-lularROSproduction.Conclusion GLP-1mayprotect H9 C2 cardiomyocytes against AGEs-induced injury partly by inhibiting excessive autophagy.关键词
胰高血糖素样肽素-1/糖基化终产物/H9C2心肌细胞/自噬/活性氧/细胞保护Key words
GLP-1/AGEs/H9 C2 cardiomyocytes/Au-tophagy/ROS/myocardial preservation分类
医药卫生引用本文复制引用
张军,谷翔,黄问银,张普华,于欢,殷嫦嫦,王丽丽,毛卫未..胰高血糖素样肽-1对AGEs诱导H9 C2心肌细胞自噬的影响[J].中国药理学通报,2017,33(3):348-353,6.基金项目
国家自然科学(地区)基金项目(No 81660152) （地区）
江西省教育厅科技项目(No GJJ09350) （No GJJ09350）
