Publication | Open Access
Role of zinc oxide nanoparticles in alleviating hepatic fibrosis and nephrotoxicity induced by thioacetamide in rats
84
Citations
29
References
2017
Year
Lipid PeroxidationRenal InflammationNanotoxicologyHepatic FibrosisRedox BiologyOxidative StressInflammationNanomedicineTaa ToxicityToxicologyHepatotoxicityHealth SciencesBiochemistryLiver PhysiologyReactive Oxygen SpecieMicronutrientsPharmacologyDrug-induced Liver InjuryHepatologyPhysiologyLiver DiseaseTaa TreatmentZinc Oxide NanoparticlesMedicine
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.
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