| Abstract |
The increasing role of copper oxide nanoparticles (CuO-NPs) in many industries and their broad range of applications increase their potential toxic effects. Quercetin (QC) is one of the most abundant dietary flavonoids found in fruits and vegetables. QC has anti-infammatory, antioxidant and anti-apoptotic properties. Echinacea purpurea (E. purpurea) is a perennial herbaceous plant that has anti-inflammatory and antioxidant properties. This study was aimed to evaluate the role of QC and E. purpurea in attenuating CuO-NPs induced hepato-renal toxicity. A total of forty-two adult male Albino rats were distributed equally into six groups. The first group (G1) received saline daily via stomach tube. G2 was administered QC at a dose of 100mg/kg b.wt. daily via stomach tube. G3 was administered E. purpurea at a dose of 150mg/kg b.wt. daily via stomach tube. G4 was given CuO-NPs at a dose of 300mg/kg b.wt. daily by stomach tube. G5 was given CuO-NPs and QC daily at the same dose and route. G6 was administered CuO-NPs and E. purpurea daily at the same dose and route. After four weeks of the experiment, blood, liver and kidney samples were obtained from rats in all experiment groups. Through improvements in serum ALT, AST, and ALP, the results demonstrated that QC and E. purpurea mitigated the hepatic dysfunctions caused by CuO-NPs, with a significant decrease of total proteins and albumin levels. E. purpurea ameliorated renal dysfunctions through improving serum creatinine (CRE), urea, and uric acid levels. QC and E. purpurea increased levels of reduced glutathione (GSH), catalase (CAT), The increasing role of copper oxide nanoparticles (CuO-NPs) in many industries and their broad range of applications increase their potential toxic effects. Quercetin (QC) is one of the most abundant dietary flavonoids found in fruits and vegetables. QC has anti-infammatory, antioxidant and anti-apoptotic properties. Echinacea purpurea (E. purpurea) is a perennial herbaceous plant that has anti-inflammatory and antioxidant properties. This study was aimed to evaluate the role of QC and E. purpurea in attenuating CuO-NPs induced hepato-renal toxicity. A total of forty-two adult male Albino rats were distributed equally into six groups. The first group (G1) received saline daily via stomach tube. G2 was administered QC at a dose of 100mg/kg b.wt. daily via stomach tube. G3 was administered E. purpurea at a dose of 150mg/kg b.wt. daily via stomach tube. G4 was given CuO-NPs at a dose of 300mg/kg b.wt. daily by stomach tube. G5 was given CuO-NPs and QC daily at the same dose and route. G6 was administered CuO-NPs and E. purpurea daily at the same dose and route. After four weeks of the experiment, blood, liver and kidney samples were obtained from rats in all experiment groups. Through improvements in serum ALT, AST, and ALP, the results demonstrated that QC and E. purpurea mitigated the hepatic dysfunctions caused by CuO-NPs, with a significant decrease of total proteins and albumin levels. E. purpurea ameliorated renal dysfunctions through improving serum creatinine (CRE), urea, and uric acid levels. QC and E. purpurea increased levels of reduced glutathione (GSH), catalase (CAT), and lowered levels of malondialdehyde (MDA) in the co-treated groups compared to CuO-NPs group.
QC and E. purpurea decreased the apoptotic effect of CuO-NPs by significantly down-regulated mRNA expressions of nuclear factor kappa B (NFκB), signal transducer and activator of transcription (STAT-3) genes and up-regulated mRNA expressions of phosphoinositide 3-kinase (PI3K), AKT (protein kinase B) genes in the liver and kidney tissue, respectively. Additionally, QC and E. purpurea preserved the architecture of hepato-renal tissue, decreased the immunoreactivity against caspase-3 (Cas-3). These findings suggest that QC has hepatoprotective effects and E. purpurea has nephroprotective and hepatoprotective effects against oxidative stress and apoptosis caused by CuO-NPs toxicity.
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