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Research Articles

Intranasal galantamine/chitosan complex nanoparticles elicit neuroprotection potentials in rat brains via antioxidant effect

, , & ORCID Icon
Pages 735-740 | Received 06 Oct 2020, Accepted 16 May 2021, Published online: 07 Jun 2021
 

Abstract

Background

Alzheimer’s disease is a common cause of dementia in the elderly. Galantamine hydrobromide (GH) is an anti-Alzheimer cholinesterase inhibitor that has an intrinsic antioxidant effect. In a previous study, GH was complexed with chitosan to prepare intranasal GH/chitosan complex nanoparticles (CX-NP2). The nanoparticles were located in rat brains 1 h after nasal administration and showed pharmacological superiority to GH nasal solution without showing histopathological toxicity.

Objective

This study aimed to investigate whether the long-term administration of CX-NP2 leads to biochemical toxicity in rat brains compared to GH nasal solution.

Methods

CX-NP2 dispersion and GH solution were administrated intranasally to male Wistar rats for 30 days (3 mg/kg/day). Malondialdehyde (MDA), lipid peroxidation marker, glutathione (GSH), superoxide dismutase (SOD) activity and tumor necrosis factor-α (TNF-α) were assessed in the brain extracts in all groups.

Results

There was statistically insignificant difference between the CX-NP2 and GH nasal solution treated groups in all biochemical toxicity parameters assessed. Interestingly, MDA and TNF-α levels in the CX-NP2-treated group significantly decreased compared to the control group. Also, GSH level and SOD activity were significantly enhanced in CX-NP2 treated group compared to the control group.

Conclusions

CX-NP2 did not induce a statistically significant oxidative stress or neuroinflammation in rat brains after 30-day treatment, they rather elicited neuroprotective potentials.

    Highlights

  • Intranasal GH/chitosan complex nanoparticles (CX-NP2) show promising potential as a brain targeting carrier.

  • Compared to GH nasal solution, nasal CX-NP2 formulation did not exert oxidative stress nor neuroinflammation when administered for 30 days.

Correction Statement

This article has been corrected with minor changes. These changes do not impact the academic content of the article.

Acknowledgement

The authors report no acknowledgements for financial or editorial support.

Disclosure statement

The authors declare no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

Additional information

Funding

This study was funded by the authors themselves.

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