Elmongy Noura Fathy, Meawad Samah Baleegh, Elshora Shimaa Zakaria, Atwa Asmaa Huessiny, Hammad Amal Mahmoud, Mehanna Osama Mahmoud, Ashry Walaa Mohamed
Physiology Department, Damietta Faculty of Medicine, Al-Azhar University, Damietta, Egypt.
Forensic Medicine and Clinical Toxicology Department, Faculty of Medicine, Al-Azhar University, Cairo, Egypt.
J Biochem Mol Toxicol. 2023 Sep;37(9):e23420. doi: 10.1002/jbt.23420. Epub 2023 Jun 22.
The 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.
银以各种形式的广泛使用引发了对其潜在不良影响的担忧。银纳米颗粒（AgNPs）可进入大脑并随后诱发神经毒性。作为多种生长因子的来源及其细胞保护特性，富血小板血浆（PRP）在再生医学中受到了相当大的关注。我们的目的是评估AgNPs对大鼠大脑的毒性作用，并评估PRP对AgNPs诱导的神经毒性的可能保护作用。总共40只成年雄性大鼠被分为四组（n = 10），即对照组、AgNPs组、AgNPs + PRP组和自动恢复组。AgNPs以10 mg/kg体重的剂量腹腔内注射（i.p.），每天一次，共28天。PRP在AgNPs治疗一天后腹腔内注射，剂量为0.5 mL/kg体重，每周两次，共3周。自动恢复组的大鼠在AgNP毒性作用后3周不进行治疗。收集血清和脑组织样本以评估促炎细胞因子、氧化应激标志物以及凋亡标志物的表达水平。进行了脑组织病理学和免疫组织化学检查。AgNPs显著增加了氧化应激标志物和促炎细胞因子，降低了抗氧化防御标志物，并诱导了凋亡和脑组织病理学损伤。然而，PRP治疗恢复了大脑氧化/抗氧化平衡，减轻了炎症状态，预防了凋亡，并改善了由AgNPs诱导的脑组织病理学损伤，自动恢复组未显示出明显改善。我们的数据为PRP对AgNPs诱导的神经毒性提供了一种新的保护作用，这归因于其抗氧化、抗炎和抗凋亡作用。
