摘要
目的:探讨磷酸肌酸钠对阿霉素所致小鼠心肌损伤的保护作用及机制。方法:60只雌性BALB/c小鼠随机分为磷酸肌酸钠干预组、阿霉素组和正常对照组,观察小鼠的一般情况,检测血清中肌钙蛋白I(TnI)、N端前脑钠肽(NT-proBNP)及心肌组织中丙二醛(MDA)、ATP酶的变化,心肌细胞凋亡及心肌组织bcl-2、fas基因的表达。结果:与对照组及磷酸肌酸钠组比较,阿霉素组心肌细胞发生明显的水肿变性,并可见部分细胞凋亡,凋亡指数增大(P<0.05);阿霉素组MDA明显增高(P<0.05),ATP酶活力降低(P<0.05);血清中TnI和NT-proBNP有增高的趋势(P>0.05);磷酸肌酸钠组与阿霉素组比较,bcl-2基因表达增多,fas基因表达减少(P<0.05)。结论:磷酸肌酸钠对阿霉素所致的心肌损伤具有保护作用,其机制可能与磷酸肌酸钠减少氧自由基和抑制细胞凋亡有关。
AIM： To observe the effect of sodium phosphocreatine on adriamycin-induced cardiotoxicity in mice.METHODS： Sixty female BALB/c mice weighing about 20 g were randomly divided into control group,adriamycin group and sodium phosphocreatine treatment group.The general conditions of the mice were observed.The content of amino-terminal pro-brain natriuretic peptide（NT-proBNP） and troponin I（TnI） in serum,the changes of malondialdehyde（MDA） concentration and ATPase activity in cardiac tissues were detected.The anti-apoptotic effect of sodium phosphocreatine was also evaluated by in situ terminal dUTP nick-end labeling（TUNEL）.The mRNA levels of bcl-2 and fas were detected by RT-PCR.RESULTS： The intracellular edema,nuclear degeneration and apoptosis were observed in the cardiac tissues in adriamycin-treated mice.Compared with control group and sodium phosphocreatine treatment group,the apoptosis index was increased,the MDA concentrations were elevated and the activity of ATPase was decreased in mouse cardiac tissues in adriamycin group.The serum levels of TnI and NT-proBNP were increased,the expression of bcl-2 was promoted and the expression of fas was inhibited in sodium phosphocreatine treatment group as compared to adriamycin group.CONCLUSION： Sodium phosphocreatine protects mice from adriamycin-induced cardiotoxicity by reduction of oxygen free radicals and apoptosis in mouse cardiac tissues.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2011年第5期939-943,共5页
Chinese Journal of Pathophysiology
基金
安徽省高等学校省级自然科学基金资助项目(No.KJ2010B252)
关键词
磷酸肌酸钠
阿霉素
细胞凋亡
自由基
Sodium phosphocreatine
Adriamycin
Apoptosis
Free radicals
