Salwa Ali Zein El Abedeen
Asst. Professor
Quercetin Abrogates Oxidative Neurotoxicity Induced by Silver Nanoparticles in Wistar Rats
• 2023
Publication Information
Authors
Samar S. Elblehi 1, Eman M. Abd El-Maksoud 2, Adil Aldhahrani 3, Saqer S. Alotaibi 4 , Heba I. Ghamry 5 ,
Salwa A. Elgendy 6, Mohamed Mohamed Soliman 3 and Mustafa Shukry 7,*
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publication.type
Local
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Abstract
This study aimed to investigate the oxidative neurotoxicity induced by silver nanoparticles
(AgNPs) and assess the neuroprotective effects of quercetin against this toxicity. Forty adult male
rats were divided into four equal groups: control, AgNPs (50 mg/kg intraperitoneally), quercetin
(50 mg/kg orally), and quercetin + AgNPs. After 30 days, blood and brain tissue samples were
collected for further studies. AgNP exposure increased lipid peroxidation and decreased glutathione
peroxidase, catalase, and superoxide dismutase activities in brain tissue. AgNPs decreased serum
acetylcholine esterase activity and
-aminobutyric acid concentrations. AgNPs upregulated tumor
necrosis factor- , interleukin-1 , and Bax transcript levels. AgNPs reduced the transcripts of claudin-
5, brain-derived neurotrophic factor, paraoxonase, nuclear factor-erythroid factor 2 (Nrf2), and Bcl-2.
Histopathologically, AgNPs caused various degenerative changes and neuronal necrosis associated
with glial cell reactions. AgNPs increased the immunohistochemical staining of glial fibrillary
acidic protein (GFAP) in the cerebrum and cerebellum. Oral treatment with quercetin efficiently
counteracted the opposing effects of AgNPs on brain tissue via modulation of tight junction proteins,
Nrf2, and paraoxonase, and its positive mechanism in modulating pro-inflammatory cytokines and
the downregulation of GFAP expression, and the apoptotic pathway. AgNPs also altered the severity
of histopathological lesions and modulated GFAP immunostaining in the examined tissue.
(AgNPs) and assess the neuroprotective effects of quercetin against this toxicity. Forty adult male
rats were divided into four equal groups: control, AgNPs (50 mg/kg intraperitoneally), quercetin
(50 mg/kg orally), and quercetin + AgNPs. After 30 days, blood and brain tissue samples were
collected for further studies. AgNP exposure increased lipid peroxidation and decreased glutathione
peroxidase, catalase, and superoxide dismutase activities in brain tissue. AgNPs decreased serum
acetylcholine esterase activity and
-aminobutyric acid concentrations. AgNPs upregulated tumor
necrosis factor- , interleukin-1 , and Bax transcript levels. AgNPs reduced the transcripts of claudin-
5, brain-derived neurotrophic factor, paraoxonase, nuclear factor-erythroid factor 2 (Nrf2), and Bcl-2.
Histopathologically, AgNPs caused various degenerative changes and neuronal necrosis associated
with glial cell reactions. AgNPs increased the immunohistochemical staining of glial fibrillary
acidic protein (GFAP) in the cerebrum and cerebellum. Oral treatment with quercetin efficiently
counteracted the opposing effects of AgNPs on brain tissue via modulation of tight junction proteins,
Nrf2, and paraoxonase, and its positive mechanism in modulating pro-inflammatory cytokines and
the downregulation of GFAP expression, and the apoptotic pathway. AgNPs also altered the severity
of histopathological lesions and modulated GFAP immunostaining in the examined tissue.