首页|阿托伐他汀改善阿霉素扩张型心肌病大鼠心肌能量代谢

阿托伐他汀改善阿霉素扩张型心肌病大鼠心肌能量代谢

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目的 探讨阿托伐他汀对阿霉素扩张型心肌病(DCM)大鼠心肌能量代谢的影响。方法 采用2。5 mg/kg阿霉素诱导DCM大鼠模型。Wistar大鼠分为对照组、DCM组、DCM+阿托伐他汀组(atf-DCM组)。比较各组大鼠第7 周心脏结构和功能、心脏体积和质量;HE染色观察大鼠心肌组织病理形态学变化;Western blotting检测大鼠心肌组织过氧化物酶体增殖物激活受体α(PPARα)、PPAR协同刺激因子-1α(PGC-1α)、腺嘌呤核苷酸转运体(ANT)蛋白表达水平。结果 与对照组比较,DCM组大鼠心脏质量增加,atf-DCM组可部分逆转上述趋势(P<0。01)。DCM组大鼠心脏体积大于对照组(P<0。01)。atf-DCM组心脏结构和功能均优于DCM组,但未达到对照组水平,各组间差异无显著性(P>0。05)。HE染色结果发现,DCM组大鼠左心室部分肌原纤维发生了溶解,心肌细胞间隙增加,心肌纤维出现断裂,有空泡产生;atf-DCM组心肌纤维断裂情况缓解,心肌细胞间隙无明显增加,空泡变性不明显。心肌PPARα、PGC-1α和ANT蛋白水平DCM组低于对照组,atf-DCM组高于DCM组(P<0。01)。结论 阿托伐他汀可上调DCM大鼠心肌PPARα、PGC-1α和ANT蛋白水平,改善心肌能量代谢,从而改善大鼠心脏功能。
Atorvastatin improves myocardial energy metabolism in adriamycin-induced dilated cardio-myopathy rats
Aim To investigate the effect of atorvastatin on myocardial energy metabolism in adriamycin dilated cardiomyop-athy(DCM)rats.Methods DCM rat model was induced by 2.5 mg/kg adriamycin.Wistar rats were divided into control group,DCM group,and DCM+atorvastatin group(atf-DCM group).Cardiac structure and function,volume and mass were compared at the 7th week in each group;HE staining was used to observe the pathomorphological changes of rat myocardial tissue;Western blotting was used to detect the protein expression levels of peroxisome proliferator-activated receptor α(PPARα),PPAR cos-timulatory factor-1α(PGC-1α),and adenine nucleotide transporter(ANT)in rat myocardial tissue.Results Compared with the control group,the heart mass of DCM group increased,and atf-DCM group reversed the above trend(P<0.01).The heart volume of DCM rats was larger than that of control group(P<0.01).Cardiac structure and function were better in atf-DCM group than in DCM group,but did not reach the level of control group,and there was no significant difference between the groups(P>0.05).HE stai-ning showed that some myofibrils in the left ventricle of DCM group were dissolved,the myocardial cell space was increased,the myo-cardial fibers were broken,and vacuoles were produced;in the atf-DCM group,the myocardial fiber breakage was relieved,the myo-cardial cell space was not significantly increased,and vacuolar degeneration was not obvious.Myocardial PPARα,PGC-1α and ANT protein levels were lower in the DCM group than in the control group and higher in the atf-DCM group than in the DCM group(P<0.01).Conclusion Atorvastatin can up-regulate myocardial PPARα,PGC-1α and ANT protein levels,improve myocardial en-ergy metabolism,and thus improve cardiac function in DCM rats.

DCMatorvastatinenergy metabolismPPARαPGC-1αANTrats

季朝红、袁博、魏文扬、刘少辉、王鑫

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西安市第九医院心血管病院一科,陕西西安 710054

DCM 阿托伐他汀 能量代谢 PPARα PGC-1α ANT 大鼠

陕西省自然科学基础研究计划西安市第九医院研究项目

2022JM-5802020-10

2024

中南医学科学杂志
南华大学

中南医学科学杂志

CSTPCD
影响因子:0.757
ISSN:2095-1116
年,卷(期):2024.52(2)
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