Platelet‐rich plasma ameliorates neurotoxicity induced by silver nanoparticles in male rats via modulation of apoptosis, inflammation, and oxidative stress

Author:

Elmongy Noura Fathy1ORCID,Meawad Samah Baleegh2,Elshora Shimaa Zakaria3,Atwa Asmaa Huessiny2,Hammad Amal Mahmoud4,Mehanna Osama Mahmoud1ORCID,Ashry Walaa Mohamed5ORCID

Affiliation:

1. Physiology Department, Damietta Faculty of Medicine Al‐Azhar University Damietta Egypt

2. Forensic Medicine and Clinical Toxicology Department, Faculty of Medicine Al‐Azhar University Cairo Egypt

3. Histology Department, Faculty of Medicine Al‐Azhar University Cairo Egypt

4. Biochemistry Department, Damietta Faculty of Medicine Al‐Azhar University Damietta Egypt

5. Microbiology and immunology Department, Damietta Faculty of Medicine Al‐Azhar University Damietta Egypt

Abstract

AbstractThe widespread use of silver in various forms raises concerns about its potential adverse effects. Silver nanoparticles (AgNPs) can enter the brain and subsequently induce neurotoxicity. As a source of diverse growth factors and for its cytoprotective properties, platelet‐rich plasma (PRP) has received considerable attention in regenerative medicine. Our aim was to estimate the toxic effects of AgNPs on the rat brain and assess the possible protective effects of PRP against AgNPs induced neurotoxicity. A total of 40 adult male rats were divided into four groups (n = 10), namely the control, AgNPs, AgNPs+PRP, and auto‐recovery groups. AgNPs were given intraperitoneally (i.p.) at a 10 mg/kg dose.bw daily for 28 days. PRP was given (a day after AgNPs treatment) i.p. at a dose of 0.5 mL/kg.bw twice weekly for 3 weeks. Rats in the auto‐recovery group were left without treatment for 3 weeks after AgNP toxicity. Serum and brain tissue samples were collected for assessment of proinflammatory cytokines, oxidative stress markers, as well as the expression levels of apoptotic markers. Brain histopathological and immunohistochemistry examinations were done. AgNPs significantly increased oxidative stress markers and proinflammatory cytokines, decreased antioxidant defense markers, and induced apoptosis and histopathological brain injuries. However, PRP treatment restored brain oxidant/antioxidant balance, attenuated the inflammatory state, prevented apoptosis, and improved the brain histopathological lesions induced by AgNPs, with no significant improvements shown by auto‐recovery group. Our data provided a novel protective effect for PRP against AgNPs‐induced neurotoxicity due to its antioxidant, anti‐inflammatory, and antiapoptotic effects.

Publisher

Wiley

Subject

Health, Toxicology and Mutagenesis,Toxicology,Molecular Biology,Molecular Medicine,Biochemistry,General Medicine

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