Abstract

Introduction

Drug-induced myopathy is among the most common causes of muscle disease. Lipid-lowering drugs, primarily the statins as inhibitors of the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, are a common cause of myopathy. Statin-fibrate combination potentially increases risk for myopathy and rhabdomyolysis. Blood levels of the enzymes creatine kinase (CK), aldolase and lactate dehydrogenase (LDH) increase during myopathy. Exercise may be a trigger for statin-associated muscle symptoms (SAMS).

Methods

In this study a model of myopathy induction was designed via combination of oral atorvastatin, gemfibrozil and exercise for ten days in rats. To maximise exercise, the rats were placed in a pool of water and allowed to swim before sinking in the last three days. Finally, the mean of swimming tolerance times and blood levels of creatine kinase, aldolase and lactate dehydrogenase were measured.

Results

The results showed a significantly (p < 0.05) decreased swimming tolerance time and elevated enzyme levels in rats receiving atorvastatin (ATV) and gemfibrozil (GMF) plus exercise compared with those rats in other groups. This animal model can be used to evaluate the effects of medication on reduction of statin/fibrate-induced myopathy.

中文翻译：

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阿托伐他汀和吉非贝齐联合体力活动：他汀/贝特类药物诱导的肌病动物模型

摘要

介绍

药物性肌病是肌肉疾病的最常见原因之一。降脂药物，主要是作为 3-羟基-3-甲基戊二酰辅酶 A (HMG-CoA) 还原酶抑制剂的他汀类药物，是肌病的常见原因。他汀-贝特组合可能会增加肌病和横纹肌溶解症的风险。在肌病期间，肌酸激酶 (CK)、醛缩酶和乳酸脱氢酶 (LDH) 的血液水平升高。运动可能是他汀类药物相关肌肉症状 (SAMS) 的诱因。

方法

在这项研究中，通过口服阿托伐他汀、吉非贝齐和运动 10 天的组合在大鼠中设计了肌病诱导模型。为了最大限度地锻炼，大鼠被放置在水池中，并在最后三天下沉之前允许其游泳。最后，测量游泳耐受时间的平均值和肌酸激酶、醛缩酶和乳酸脱氢酶的血液水平。

结果

结果显示， 与其他组的大鼠相比，接受阿托伐他汀 (ATV) 和吉非罗齐 (GMF) 加运动的大鼠的游泳耐受时间显着降低 ( p < 0.05)，酶水平升高。该动物模型可用于评估药物对减少他汀类药物/贝特类诱发的肌病的影响。