摘要
目的研究HO-1对脂多糖刺激的心肌细胞内钙离子含量的影响。方法差速贴壁法培养乳鼠心肌细胞,分为对照组(C),脂多糖LPS组(L),LPS+Hemin组(L+H),LPS+ZnPP组(L+Zn),分别诱导或阻断HO-1的合成,并检测心肌细胞内钙离子含量。结果 LPS诱导心肌细胞钙离子含量升高,Hemin增加HO-1水平,降低细胞内钙离子水平,ZnPP降低HO-1水平,细胞内钙离子浓度进一步增加。结论 LPS刺激使心肌细胞内钙离子含量明显升高,HO-1可降低细胞内钙超载。
Objective Heme oxygenase-1 （HO-1）,the rate-limiting enzyme in heme catabolism,has been shown to be induced in inflammatory disease,and acts as an important cellular defense mechanism against cell injury.In this study,the effect of HO-1 on Ca2＋ was studied in a model of lipopolysaccharide-induced acute cardiocyte injury.Methods Cardiocyte was cultured with different adherence,and was enrolled into group control,group of LPS＋Hemin（L＋H）,and group of LPS＋ZnPP （L＋Zn）.The level of HO-1 and Ca2＋ was measured with RT-PCR,Western blotting and flow cytometry,respectively.Results We found that LPS treatment of cardiocyte resulted in severe increase of Ca2＋.Whereas upregulation of HO-1 by hemin pretreatment decreased the level of Ca2＋.Inhibition of HO-1 activity by zinc protoporphyrin-9 （ZnPP,a specific inhibitor of HO） make the level of Ca2＋ more high.Conclusion These data therefore showed that the level of Ca2＋ was increased in the model of LPS-induced acute cardiocyte injury.This change can be inhibited by HO-1 partly.
出处
《江西医药》
CAS
2010年第7期644-646,共3页
Jiangxi Medical Journal
基金
国家科技支撑计划(课题号2008BAI68B02)
