Nanoparticle zinc oxide obviates oxidative stress of liver cells in induced-diabetes mellitus model

Document Type : Original article

Authors

1 Department of Clinical Trial Research Unit and Drug Discovery, Egyptian Liver Research Institute and Hospital (ELRIAH), Mansoura, Egypt.

2 Colleague Medical Research Institute, Department of Applied Medical Chemistry, Medical Research Institute, Alexandria University, Alexandria, Egypt.

3 Department of Botany and Microbiology, Faculty of Science, Benha University, Benha 33516, Egypt.

4 Biochemistry Division, Chemistry Department, Faculty of Science, Zagazig University 44519

5 Faculty of Dentistry, Mansoura University, Mansoura, Egypt.

6 Tropical Medicine Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.

7 Internal Medicine Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.

8 Clinical Pathology Department, Mansoura University, Mansoura, Egypt.

9 Animal Physiology, Zoology Department, Faculty of Science, Mansoura University, Mansoura, Egypt

10 Department of Anatomy, Faculty of Medicine, for Girls, Al-Azhar University, Cairo, Egypt

Abstract

Background: Because of vital features including biocompatibility, high surface reactivity, and oxidation resistance, emerging nanomedicine is well-known for its potential therapeutic prospects. The goal of this study is to see if nanoparticle zinc oxide (ZnONPs) may reduce hepatic problems and oxidative stress in rats with diabetes mellitus induced by streptozotocin (STZ).
Materials and methods: This study included 39 rats separated into three groups, each consisting of 13 rats; control group, streptozotocin group, and streptozotocin + ZnONPs group. Malondialdehyde (MDA), nitric oxide (NO), glutathione (GSH), and reactive oxygen species (ROS) were measured as biochemical-specific oxidative stress measures. Fasting blood sugar (FBS), haemoglobin A1c (HbA1C), and tumour necrosis factor (TNF-β) were also measured, as well as total cholesterol and triglycerides. The percentage of P53 in the liver was determined. Inflammatory cell infiltration and fibrosis in tissues were also seen by histological investigation. Results: FBS, HbA1C, liver function tests, MDA, NO, ROS, P53, and TNF-β serum levels were increased in STZ-treated rats. Treatment with ZnONPs (5 mg/kg) in the STZ+ ZnONPs group significantly improved, FBS, HbA1C, MDA, NO, GSH, ROS, liver function, fasting blood sugar, HbA1C, and tumour necrosis factor. In addition, ZnONPs treatment banned inflammatory cell infiltration and P53 in STZ-administered rats. Conclusion: Our study provides evidence that ZnONPs may aid in controlling hepatic oxidative stress in STZ-induced diabetes mellitus in rats.

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