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氧化锌纳米颗粒在减轻硫代乙酰胺诱导的大鼠肝纤维化和肾毒性中的作用。

Role of zinc oxide nanoparticles in alleviating hepatic fibrosis and nephrotoxicity induced by thioacetamide in rats.

作者信息

Bashandy Samir A E, Alaamer Abdulaziz, Moussa Sherif A Abdelmottaleb, Omara Enayat A

机构信息

a Department of Pharmacology, Medical Division, National Research Centre, 33 EL Bohouth St. (former EL Tahir St.), Dokki, Giza, Egypt. P.O.12622.

b Committee of Radiation and Environmental Pollution Protection (CREPP), Department of Physics, College of Science, Al-Imam Mohammad Ibn Saud Islamic University (IMSIU), Riyadh, Saudi Arabia.

出版信息

Can J Physiol Pharmacol. 2018 Apr;96(4):337-344. doi: 10.1139/cjpp-2017-0247. Epub 2017 Aug 16.

Abstract

The present research studied the influence of zinc oxide nanoparticles (ZnO-NPs; 5, 7.5, and 10 mg/kg, i.p.) on the liver and kidney injuries motivated by thioacetamide (TAA; 100 mg/kg, i.p.). Each treatment was carried out 3 times per week for 8 weeks. ZnO-NPs relieved the decrease of hepatic or renal reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) induced by TAA. Moreover, ZnO-NPs lowered tissue malondialdehyde (MDA, an indicator for lipid peroxidation). TAA treatment led to a significant increase in plasma inflammatory markers (TNF-α, IL-6), liver enzymes (gamma-glutamyltransferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and kidney function parameters (creatinine, urea, uric acid). However, these parameters were reduced after treatment with ZnO-NPs. In addition, the hepatic fibrosis markers, hydroxyproline level, and α-smooth muscle actin immunopositive stain were lowered by ZnO-NPs. The protective effect of ZnO-NPs in respect to biochemical changes was also confirmed by histopathological and immunohistochemistry studies in the liver and kidney sections. Our results suggested that ZnO-NPs may attenuate TAA toxicity via suppression of oxidative stress.

摘要

本研究探讨了纳米氧化锌(ZnO-NPs;腹腔注射剂量为5、7.5和10 mg/kg)对硫代乙酰胺(TAA;腹腔注射剂量为100 mg/kg)所致肝损伤和肾损伤的影响。每周进行3次治疗,持续8周。ZnO-NPs缓解了TAA诱导的肝脏或肾脏中还原型谷胱甘肽(GSH)、过氧化氢酶(CAT)和超氧化物歧化酶(SOD)的减少。此外,ZnO-NPs降低了组织丙二醛(MDA,脂质过氧化指标)。TAA治疗导致血浆炎症标志物(TNF-α、IL-6)、肝酶(γ-谷氨酰转移酶(GGT)、天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT))以及肾功能参数(肌酐、尿素、尿酸)显著升高。然而,用ZnO-NPs治疗后这些参数降低。此外,ZnO-NPs降低了肝纤维化标志物、羟脯氨酸水平以及α-平滑肌肌动蛋白免疫阳性染色。肝和肾切片的组织病理学和免疫组织化学研究也证实了ZnO-NPs在生化变化方面的保护作用。我们的结果表明,ZnO-NPs可能通过抑制氧化应激来减轻TAA毒性。

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