Yasser Ashry Khadrawy, Eman Nasr Hosny, Haitham Sharf Eldein Mohamed
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The concentration of dopamine (DA), norepinephrine (NE), serotonin (5-HT), lipid peroxidation (MDA), reduced glutathione (GSH), and nitric oxide (NO), and the activities of Na<sup>+</sup>,K<sup>+</sup>,ATPase, acetylcholinesterase (AchE), and monoamine oxidase (MAO) were determined in the midbrain and striatum. Data were analyzed by ANOVA at <i>P</i>-value<0.05.</p><p><strong>Results: </strong>The PD model exhibited a decrease in motor activity. In the midbrain and striatum of the PD model, DA, NE, and 5-HT levels decreased significantly (<i>P</i>-value<0.05). However, an increase in MAO, NO, and MDA was observed. GSH, AchE and Na<sup>+</sup>,K<sup>+</sup>,ATPase decreased significantly in the two brain areas. FeONPs-Cur prevented the decline of dopamine and norepinephrine and reduced oxidative stress in both areas. It also prevented the increased MAO activity in the two areas and the inhibited activity of AchE and Na<sup>+</sup>,K<sup>+</sup>,ATPase in the midbrain. These changes were associated with improvements in motor activity.</p><p><strong>Conclusion: </strong>The present data indicate that FeONPs-Cur could prevent the motor deficits induced in the PD rat model by restoring dopamine and norepinephrine in the midbrain and striatum. The antioxidant activity of FeONPs-Cur contributed to its protective effect. 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The open field test was used to assess motor activity. The concentration of dopamine (DA), norepinephrine (NE), serotonin (5-HT), lipid peroxidation (MDA), reduced glutathione (GSH), and nitric oxide (NO), and the activities of Na<sup>+</sup>,K<sup>+</sup>,ATPase, acetylcholinesterase (AchE), and monoamine oxidase (MAO) were determined in the midbrain and striatum. Data were analyzed by ANOVA at <i>P</i>-value<0.05.</p><p><strong>Results: </strong>The PD model exhibited a decrease in motor activity. In the midbrain and striatum of the PD model, DA, NE, and 5-HT levels decreased significantly (<i>P</i>-value<0.05). However, an increase in MAO, NO, and MDA was observed. GSH, AchE and Na<sup>+</sup>,K<sup>+</sup>,ATPase decreased significantly in the two brain areas. FeONPs-Cur prevented the decline of dopamine and norepinephrine and reduced oxidative stress in both areas. 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引用次数: 0
摘要
研究目的本研究旨在探讨姜黄素包裹的氧化铁纳米颗粒(FeONPs-Cur)对雷舍平诱导的帕金森病(PD)模型大鼠运动障碍和神经化学变化的保护作用:将大鼠分为对照组、利血平诱导的帕金森病模型组和用 FeONPs-Cur 治疗的帕金森病模型组(8 只/组)。开阔地试验用于评估大鼠的运动活动。测定中脑和纹状体中多巴胺(DA)、去甲肾上腺素(NE)、5-羟色胺(5-HT)、脂质过氧化物(MDA)、还原型谷胱甘肽(GSH)和一氧化氮(NO)的浓度,以及Na+、K+、ATP酶、乙酰胆碱酯酶(AchE)和单胺氧化酶(MAO)的活性。数据按 P 值进行方差分析:帕金森病模型的运动活动减少。在 PD 模型的中脑和纹状体中,DA、NE 和 5-HT 水平显著下降(P-value+),K+、ATPase 在这两个脑区显著下降。FeONPs-Cur阻止了多巴胺和去甲肾上腺素的下降,并降低了这两个区域的氧化应激。它还防止了这两个区域中 MAO 活性的增加以及中脑中 AchE 和 Na+,K+,ATPase 活性的抑制。这些变化与运动活动的改善有关:本研究数据表明,FeONPs-Cur 可通过恢复中脑和纹状体中的多巴胺和去甲肾上腺素来预防帕金森病大鼠模型的运动障碍。FeONPs-Cur的抗氧化活性有助于其保护作用。这些作用使FeONPs-Cur成为抗帕金森病的候选药物。
Assessment of the neuroprotective effect of green synthesized iron oxide nanoparticles capped with curcumin against a rat model of Parkinson's disease.
Objectives: The current study aims to investigate the protective effect of iron oxide nanoparticles capped with curcumin (FeONPs-Cur) against motor impairment and neurochemical changes in a rat model of Parkinson's disease (PD) induced by reserpine.
Materials and methods: Rats were grouped into control, PD model induced by reserpine, and PD model treated with FeONPs-Cur (8 rats/group). The open field test was used to assess motor activity. The concentration of dopamine (DA), norepinephrine (NE), serotonin (5-HT), lipid peroxidation (MDA), reduced glutathione (GSH), and nitric oxide (NO), and the activities of Na+,K+,ATPase, acetylcholinesterase (AchE), and monoamine oxidase (MAO) were determined in the midbrain and striatum. Data were analyzed by ANOVA at P-value<0.05.
Results: The PD model exhibited a decrease in motor activity. In the midbrain and striatum of the PD model, DA, NE, and 5-HT levels decreased significantly (P-value<0.05). However, an increase in MAO, NO, and MDA was observed. GSH, AchE and Na+,K+,ATPase decreased significantly in the two brain areas. FeONPs-Cur prevented the decline of dopamine and norepinephrine and reduced oxidative stress in both areas. It also prevented the increased MAO activity in the two areas and the inhibited activity of AchE and Na+,K+,ATPase in the midbrain. These changes were associated with improvements in motor activity.
Conclusion: The present data indicate that FeONPs-Cur could prevent the motor deficits induced in the PD rat model by restoring dopamine and norepinephrine in the midbrain and striatum. The antioxidant activity of FeONPs-Cur contributed to its protective effect. These effects nominate FeONPs-Cur as an antiparkinsonian candidate.
期刊介绍:
The Iranian Journal of Basic Medical Sciences (IJBMS) is a peer-reviewed, monthly publication by Mashhad University of Medical Sciences (MUMS), Mashhad, Iran . The Journal of "IJBMS” is a modern forum for scientific communication. Data and information, useful to investigators in any discipline in basic medical sciences mainly including Anatomical Sciences, Biochemistry, Genetics, Immunology, Microbiology, Pathology, Pharmacology, Pharmaceutical Sciences, and Physiology, will be published after they have been peer reviewed. This will also include reviews and multidisciplinary research.