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. 2024;27(1):81-89.
doi: 10.22038/IJBMS.2023.73124.15892.

Assessment of the neuroprotective effect of green synthesized iron oxide nanoparticles capped with curcumin against a rat model of Parkinson's disease

Affiliations

Assessment of the neuroprotective effect of green synthesized iron oxide nanoparticles capped with curcumin against a rat model of Parkinson's disease

Yasser Ashry Khadrawy et al. Iran J Basic Med Sci. 2024.

Abstract

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.

Keywords: FeONPs-Cur; Monoamines; Motor activity; Oxidative stress; Parkinson’s disease.

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Conflict of interest statement

None.

Figures

Figure 1
Figure 1
Effect of daily treatment with FeONPs-Cur (5 mg/kg/day for 14 days) on the open field test parameters (Number of crossed lines, Number of rearings Time spent in the central square, and Freezing time) in the reserpine-induced PD rat model
Figure 2
Figure 2
Effect of daily treatment with FeONPs-Cur (5 mg/kg/day for 14 days) on the level of lipid peroxidation (MDA)(mmol/g), nitric oxide (NO) (µmol/g), and reduced glutathione (GSH) (mmol/g) in the midbrain of reserpine-induced PD rat model
Figure 3
Figure 3
Effect of daily treatment with FeONPs-Cur (5 mg/kg/day for 14 days) on the level of lipid peroxidation (MDA)(mmol/g), nitric oxide (NO) (µmol/g)), and reduced glutathione (GSH) (mmol/g) in the striatum of reserpine-induced PD rat model
Figure 4
Figure 4
Effect of daily treatment with FeONPs-Cur (5 mg/kg/day for 14 days) on the activity of Na+,K+,ATPase (µmol Pi/min/g), acetylcholinesterase (AchE) (µmol SH/min/g))), and monoamine oxidase (MAO) (mU/g) in the midbrain of reserpine-induced PD rat model
Figure 5
Figure 5
Effect of daily treatment with FeONPs-Cur (5 mg/kg/day for 14 days) on the activity of Na+, K+, ATPase (µmol Pi/min/g), acetylcholinesterase (AchE) (µmol SH/min/g), and monoamine oxidase (MAO) (mU/g) in the striatum of reserpine-induced PD rat model
Figure 6
Figure 6
Effect of daily treatment with FeONPs-Cur (5 mg/kg/day for 14 days) on the level of serotonin (5-HT) (µg/g), norepinephrine (NE) (µg/g)), and dopamine (DA) (µg/g) in the midbrain of reserpine-induced PD rat model
Figure 7
Figure 7
Effect of daily treatment with FeONPs-Cur (5 mg/kg/day for 14 days) on the level of serotonin (5-HT) (µg/g), norepinephrine (NE) (µg/g)), and dopamine (DA) (µg/g) in the striatum of reserpine-induced PD rat model

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References

    1. Balestrino R, Schapira AHV. Parkinson disease. Eur J Neurol. 2020;27:27–42. - PubMed
    1. Tysnes OB, Storstein A. Epidemiology of Parkinson’s disease. J Neural Transm. 2017;124:901–905. - PubMed
    1. Ikenaka K, Suzuki M, Mochizuki H, Nagai Y. Lipids as trans-acting effectors for α-synuclein in the pathogenesis of Parkinson’s disease. Front Neurosci. 2019;13:693. - PMC - PubMed
    1. DeMaagd G, Philip A. Parkinson’s disease and its management: Part 1: disease entity, risk factors, pathophysiology, clinical presentation, and diagnosis. P T. 2015;40:504–532. - PMC - PubMed
    1. Kim GH, Kim JE, Rhie SJ, Yoon S. The role of oxidative stress in neurodegenerative diseases. Exp Neurobiol. 2015;24:325–340. - PMC - PubMed

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