磷酸肌酸钠对小鼠阿霉素心肌损伤的保护机制初探

Primary exploration on the protective effect of phosphocreatine sodium on adriamycin-induced cardiotoxicity in mice

目的:探讨磷酸肌酸钠对小鼠阿霉素心肌损伤的保护作用。方法:雌性BALB/C小鼠60只,建立阿霉素心肌病模型,随机分为磷酸肌酸钠组、阿霉素组、正常对照组。观察小鼠的一般情况,血清中心肌酶TnI、N端前脑钠肽(NT-proB-NP)及心肌组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、ATP酶及乳酸脱氢酶(LDH)的变化,心肌组织HE染色病理变化。结果:与阿霉素组比较,磷酸肌酸钠组LDH、MDA明显降低(P<0.05),SOD和ATP酶活力明显升高(P<0.05);血清NT-proBNP及TnI水平降低(P>0.05)。阿霉素组心肌组织出现明显的水肿、变性。结论:磷酸肌酸钠通过减少氧自由基对阿霉素所致的心肌损伤具有保护作用。

AIM： To observe the protective effect of phosphocreatine sodium on adriamycin-induced cardiotoxicity in mice. METHODS. 60 female BALB/C mice weighting about 20 g were randomly divided into control group （Con）, ad-riamycin group （ADR） and phosphoereatine so-dium treatment group （CP）. The general condi-tion, the serum myocardial enzymes of NT-proBNP and TnI, the changes of MDA, SOD, LDH and ATPase in cardiac tissues were detec-ted. The changes of cardiac tissues were ob-served by HE staining. RESULTS： Compared with group ADR, the contents of MDA and LDH were reduced in mice cardiac tissues, theactivity of ATPases and SOD was elevated in mice cardiac tissues （P〈0.05） ,the serum levels of TnI and NT-proBNP were decreased in group CP（P〈0.05）. Intracellular edema and nuclear degeneration were obviously observed in adria-mycin-treated cardiac tissues by HE staining. CONCLUSION. Phosphocreatine sodium pro-tects mice from cardiotoxicity induced by adria-mycin. The reduction of oxygen free radicals in mice cardiac tissues may be involved in the pro-tective effect of phosphocreatine sodium.