Chitosan nanoparticles Mitigate Sodium Nitrite Neurotoxicity of Memory and Autophagy Disorders through modulation of immunohistochemical Expression of Neurocan, Beclin-1, and LC3-II.

Khattab, Nada; Ahmed, Rania Abd-ElKarim; Darwish, Sahar; Hafez, Hani

doi:10.21608/ejh.2022.143405.1700

Chitosan nanoparticles Mitigate Sodium Nitrite Neurotoxicity of Memory and Autophagy Disorders through modulation of immunohistochemical Expression of Neurocan, Beclin-1, and LC3-II.

Articles in Press

Document Type : Original Article

Authors

¹ Zoology department, faculty of Science, Suez University

² Associate Prof of Histology and Histochemistry , Zoology Dep. , Faculty of Sciences , Suez University , Suez , Egypt

³ 2Histopathology Department, National Organization for Drug Control and Research (NODCAR), Giza, Egypt.

⁴ Suez University, Faculty of Science, Zoology Department. Suez, Egypt

10.21608/ejh.2022.143405.1700

Abstract

Aim: The present paper aimed to investigate the toxicity of sodium nitrate on memory and learning disorders, brain pathology, and autophagy activity; in addition to the chitosan nanoparticles treatment impacts.
Results: The cognitive activity of novel locations and objects in place and fear of aggravated behavior with the ability for avoiding unpleasant stimulus among young rats are negatively influenced by sodium nitrite injection (80 mg/kg) without effects on their ability for new objects recognition. Additionally, the toxicity triggered highly distributed degenerated cells with acrocentric chromatin distributed and pyknosis on the CA3 hippocampus sub-region, with a significant increase of the intracellular deposits of beta amyloids and significant up-regulation of neurocan protein. In parallel, there was a defect in the autophagy process through down-regulation of both Beclin 1 and LC3-II expression in the hippocampus CA3 sub-region and dentate gyrus (DG). Meanwhile, chitosan NP enhanced not only cognitive learning and memory skills for location cognitive behavior and the ability for avoiding heat shock but also ameliorated the histopathological structure with decreased distributed degenerated cells and modulation of the autophagy proteins expression with a significant decrease for the toxic amyloids.
Conclusion: Our results suggested that CA3 may be considered an important site for controlling the cognitive location novelty and experience of novelty for objects in novel places not for detecting the novel objects; parallel with amelioration of the pathological aspects and inhibition of toxic beta-amyloid deposits. So, chitosan nanoparticles emerged with new insights for their pharmacological activity in the modulation of behavioral disorders and amputation of the toxic amyloid aggregation.

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