الفهرس 
Introduction and aim of the workOnly 14 pages are availabe for public view
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Abstract
Statins are the most effective and best tolerated agents for treating hyperlipidemia. They have been shown to reduce the risk of initial and recurrent cardiovascular events. The statins include cerivastatin drug which is the most potent, followed by (in instruction of decreasing potency), rosuvastatin, atorvastatin, simvastatin, lovastatin, pravastatin and fluvastatin. Statins, including atorvastatin (Lipitor), are the top-selling drugs in the world.
Many literatures focused on the possible side effects of statins. The most common side effect in statins users is myopathy.
This study is concerned with the description of structural changes in rat skeletal muscle following administration of different doses of atorvastatin and identification of different mechanisms involved in these changes.
In this study, 20 male albino rats were used. Rats were divided randomly into four groups; each group included 5 rats: Group I, the control group, received distilled water. Group II received 10 mg/kg/day of atorvastatin. Group III received 40 mg/kg/day of atorvastatin. Group IV received 80 mg/kg/day of atorvastatin. All treated groups received atorvastatin dissolved in distilled water by a gastric tube for 8 weeks. Vastus medialis of the quadriceps femoris muscle was taken out, rapidly fixed and processed for light microscopic, immunocytochemical and morphometrical studies.
The results of the current study revealed that:
In hematoxylin and eosin stained sections: atorvastatin administration caused degeneration of the skeletal muscle fibers with inflammatory cells infiltration. The degree of skeletal muscle degeneration increased with high doses.
In masson trichrome stained sections: atorvastatin administration caused progressive increase in the collagen fibers in the perimysium among the muscle bundles and was concomitant with the degree of muscle damage.
In Glees stained sections: there were apparent degenerative changes affecting the nerve fiber that were extensive with high doses.
Histochemical studies showed decreased succinate dehydrogenase (SDH) activity in type II skeletal muscle fibers in all treated groups and this decrease was extensive with high doses. On the other hand, SDH activity in type I muscle fibers affected only with the doses of 40, 80 mg/kg of atorvastatin.
Histochemical studies showed decreased acetylcholine esterase (AChE) activity with the doses of 40, 80 mg/kg of atorvastatin.
Immunohistochemical studies using myosin heavy chain antibodies; there was degeneration of the type II fibers with total sparing of the type I fibers with the doses of 10 or 40 mg/kg. However, affection of the type I fibers was observed in 80 mg/kg treated group.
Immunohistochemical studies showed a significant increase in the numbers of caspase 3-immuno positive muscle fiber in all treated group and these numbers increased with higher doses.