中国病理生理杂志2012，Vol.28Issue(3)：459-463,5.DOI:10.3969/j.issn.1000-4718.2012.03.013
附子多糖保护缺氧/复氧乳鼠心肌细胞及其抗内质网应激的机制研究
Fuzi polysaccharide protects neonatal rat cardiomyocytes with hypoxia-reoxygenation by inhibiting endoplasmic reticulum stress
摘要
Abstract
AIM:To invesligale whelher lhe proleclion mechanism of Fuzi polysaccharide (FPS) is relaled Lo inhibition of endoplasmic reliculum slress in cullured neonalal ral cardiomyocyles wilh hypoxia/reoxygenalion (H/R). METHODS; Cullured ral myocardial cells were divided inlo conlrol group, H/R group (hypoxia for 3 h and reoxygenalion for 6 h) and different concenlralions of FPS (0. 1 g/L, 1 g/L, 10 g/L or 20 g/L) + H/R groups. The cell survival was delecled by MTT assay and cell apoplosis of cardiomyocyles was measured by flow cylomelry using Annexin V - FITC slai-ning. The expression of glucose - regulaled prolein 78 ( GRP78 ) , CCAAT/enhancer - binding prolein homologous prolein ( CHOP) and caspase - 12 were determined by Weslern blolling. The mRNA expression of CHOP and caspase - 12 was delecled by quanlilalive PCR. RESULTS: Afler reoxygenalion, ihe expression of GRP78 , CHOP and caspase - 12 in cardiomyocyles was increased. Compared wilh H/R group, ihe expression of GRP78, CHOP and caspase - 12 in FPS + H/R groups was significantly inhibited, ihe survival rale of cardiomyocyles was increased and ihe apoplosis of cardiomyocyles was inhibited. This proleclive effecl of FPS was in a dose - dependenl manner and reached ils peak al 10 g/L. CONCLUSION; Fuzi polysaccharide prolecls cardiomyocyles from H/R injury. The mechanism is relaled lo inhibiting endoplasmic reliculum slress.关键词
附子多糖/内质网应激/缺氧/复氧损伤/心肌细胞Key words
Fuzi polysaccharide/ Endoplasmic reliculum slress/ Hypoxia/reoxygenalion injury/ Cardiomyocyles分类
医药卫生引用本文复制引用
刘颖,纪超,吴伟康..附子多糖保护缺氧/复氧乳鼠心肌细胞及其抗内质网应激的机制研究[J].中国病理生理杂志,2012,28(3):459-463,5.基金项目
广东省科技计划项目(No.2008B060600055) （No.2008B060600055）
