| 季朝红,袁博,魏文扬,刘少辉,王鑫.阿托伐他汀改善阿霉素扩张型心肌病大鼠心肌能量代谢.[J].中南医学科学杂志.,2024,(2):173-176. |
| 阿托伐他汀改善阿霉素扩张型心肌病大鼠心肌能量代谢 |
| Atorvastatin improves myocardial energy metabolism in adriamycin-induced dilated cardiomyopathy rats |
| 投稿时间：2023-04-13 修订日期：2023-08-01 |
| DOI：10.15972/j.cnki.43-1509/r.2024.02.004 |
| 中文关键词: DCM 阿托伐他汀 能量代谢 PPARα PGC-1α ANT 大鼠 [ |
| 英文关键词:DCM atorvastatin energy metabolism PPARα PGC-1α ANT rats |
| 基金项目:陕西省自然科学基础研究计划项目(2022JM-580)；西安市第九医院研究项目(2020-10) |
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| 中文摘要: |
| 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。 |
| 英文摘要: |
| AimTo investigate the effect of atorvastatin on myocardial energy metabolism in adriamycin dilated cardiomyopathy (DCM) rats. MethodsDCM 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 costimulatory factor-1α (PGC-1α), and adenine nucleotide transporter (ANT) in rat myocardial tissue. ResultsCompared 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 staining showed that some myofibrils in the left ventricle of DCM group were dissolved, the myocardial cell space was increased, the myocardial fibers were broken, and vacuoles were produced; in the atf-DCM group, the myocardial fiber breakage was relieved, the myocardial 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). ConclusionAtorvastatin can up-regulate myocardial PPARα, PGC-1α and ANT protein levels, improve myocardial energy metabolism, and thus improve cardiac function in DCM rats. |
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