瑞舒伐他汀可改善高脂饮食喂养的瑞士白化小鼠的焦虑情绪,但会通过丙二醛和钙耗竭损害骨骼肌性能

I. Abi, Stephen Oche Matthias, Elias Mkumaga Saater
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引用次数: 0

摘要

背景:高热量、高脂肪饮食(HFD)的高摄入量以及与之相关的久坐不动的生活方式与多种神经行为和神经肌肉疾病有关。本研究旨在探讨降脂药物瑞舒伐他汀(ROS)对高脂饮食小鼠焦虑行为和肌肉力量的影响:将小鼠分为四组(n=5):第 1 组(正常饲料和水);第 2 组(高脂饮食);第 3 组(高脂饮食 + ROS);第 4 组(高脂饮食 5 周,ROS 1 周)。之后,对小鼠进行高架加迷宫(EPM)试验和吊线试验(WHT)。然后将小鼠处死,匀浆化脑样本并检测神经递质和抗氧化剂。血液样本检测钙、尿酸和丙二醛(MDA):高密度脂蛋白胆固醇明显(p<0.05)增加了小鼠的焦虑感,而 ROS 则改善了焦虑感。然而,ROS 会降低肌肉强度。大脑中多巴胺和血清素的水平没有受到 ROS(如超氧化物歧化酶(SOD)和过氧化氢酶)的明显影响(p<0.05)。血清钙和 MDA 受 ROS 的影响明显降低:结论:高脂饮食会诱发动物焦虑,并改善其肌肉耐力。罗伐他汀可改善焦虑,但会降低肌肉强度,其机制可能是分别抑制了 MDA 和钙的功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Rosuvastatin ameliorates anxiety but impairs skeletal muscle performance by malondialdehyde and calcium depletion in high fat diet-fed swiss albino mice
Background: The high intake of high calorie, high fat diets (HFD) with an associatedsedentary lifestyle has been linked with a number of neurobehavioral and neuromusculardisorders. This study aimed at investigating the effect of a lipid lowering drug -Rosuvastatin (ROS) on anxiety-like behavior and muscle strength in HFD-fed mice.Methods: The animals were grouped into four (n=5); Group 1 (normal chow and water adlibitum); Group 2 (HFD ad libitum); Group 3 (HFD + ROS); Group 4 (HFD for 5 weeksthen ROS for 1 week). Thereafter, mice were subjected to elevated plus maze (EPM) testand wire hanging test (WHT). Animals were then killed and brain samples homogenizedand assayed for neurotransmitters and antioxidants. The blood samples were assayed forcalcium, uric acid and Malondialdehyde (MDA).Results: The HFD significantly (p<0.05) heightened anxiety in the mice which wasameliorated by ROS. Muscle strength was however decreased with ROS. Brain levels ofdopamine and serotonin were not significantly affected (p<0.05) by ROS likewisesuperoxide dismutase (SOD) and Catalase. Serum calcium and MDA were significantlyreduced by ROS.Conclusions: High fat diet induced anxiety in the animals and improved muscle enduranceon exertion. Rosuvastatin ameliorated the anxiety but reduced muscle strength and theproposed mechanism is suppression of MDA and Calcium functions respectively
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