Neuroprotective effect of piracetam-loaded magnetic chitosan nanoparticles against thiacloprid-induced neurotoxicity in albino rats.

Autor: Abomosallam M; Forensic Medicine and Toxicology Department, Faculty of Veterinary Medicine, Mansoura University, Mansoura, 35516, Egypt., Hendam BM; Husbandry and Development of Animal Wealth Department, Faculty of Veterinary Medicine, Mansoura University, Mansoura, 35516, Egypt., Abdallah AA; Central Agricultural Pesticides Laboratory, Agricultural Research Center, Giza, 12619, Egypt., Refaat R; Phytochemistry and Plant Systematics Department, National Research Center, Dokki, Giza, 12622, Egypt., Elshatory A; Forensic Medicine and Clinical Toxicology Department, School of Medicine, Cairo University, Cairo, 11865, Egypt., Gad El Hak HN; Zoology Department, Faculty of Science, Suez Canal University, Ismailia, Egypt. heba_ahmed@science.suez.edu.eg.
Jazyk: angličtina
Zdroj: Inflammopharmacology [Inflammopharmacology] 2023 Apr; Vol. 31 (2), pp. 943-965. Date of Electronic Publication: 2023 Feb 06.
DOI: 10.1007/s10787-023-01151-x
Abstrakt: Thiacloprid (TH) is a neurotoxic agricultural insecticide and potential food contaminant. The purpose of this study was to investigate the relationship between TH exposure and memory dysfunction in rats, as well as the potential protective effect of piracetam and piracetam-loaded magnetic chitosan nanoparticles (PMC NPs). Rats were divided into five equal groups (six rats/group). The control group received saline. Group II was treated with PMC NPs at a dose level of 200 mg/kg body weight (Bwt); Group III was treated with 1/10 LD 50 of TH (65 mg/kg Bwt); Group IV was treated with TH (65 mg/kg Bwt) and piracetam (200 mg/kg Bwt); Group V was co-treated with TH (65 mg/kg Bwt) and PMC NPs (200 mg/kg Bwt). All animal groups were dosed daily for 6 weeks by oral gavage. Footprint analysis, hanging wire test, open field test, and Y-maze test were employed to assess behavioral deficits. Animals were euthanized, and brain tissues were analyzed for oxidative stress biomarkers, proinflammatory cytokines, and gene expression levels of glial fibrillary acidic protein (GFAP), amyloid-beta precursor protein (APP), B-cell lymphoma 2 (Bcl-2), and caspase-3. Brain and sciatic nerve tissues were used for the evaluation of histopathological changes and immunohistochemical expression of tau protein and nuclear factor kappa B (NF-κB), respectively. The results revealed that TH-treated rats suffered from oxidative damage and inflammatory effect on the central and peripheral nerves. The administration of PMC NPs considerably protected against TH-induced neuronal damage, increased antioxidant enzyme activity, decreased inflammatory markers, and improved behavioral performance than the group treated with piracetam. The neuroprotective effect of PMC NPs was mediated through the inhibition of GFAP, APP, caspase-3, Tau, and NF-κB gene expression with induction of Bcl-2 expression. In conclusion, TH could induce oxidative stress, inflammatory and neurobehavior impairment in rats. However, PMC NPs administration markedly mitigated TH-induced brain toxicity, possibly via oxidative and inflammatory modulation rather than using piracetam alone.
(© 2023. The Author(s).)
Databáze: MEDLINE