Protective effects of gallic acid against nickel-induced kidney injury: impact of antioxidants and transcription factor on the incidence of nephrotoxicity

• Published in: Renal failure 2024-12, Vol.46 (1), p.2344656-2344656
• Main Authors: Alhazmi, Areej I, El-Refaei, Mohamed F, Abdallah, Eman A A
• Format: Article
• Language: English
• Subjects: Acute Kidney Injury; Acute Kidney Injury - chemically induced; Acute Kidney Injury - metabolism; Acute Kidney Injury - prevention & control; Animals; antioxidant; Antioxidants; Antioxidants - pharmacology; Antioxidants - therapeutic use; Biochemical markers; Body weight; Caspase-1; Deoxyguanosine; Gallic acid; Gallic Acid - pharmacology; Gallic Acid - therapeutic use; Immunohistochemistry; Kidney - drug effects; Kidney - metabolism; Kidney - pathology; Kidney diseases; Kidneys; Male; Mice; Nanoparticles; nephrotoxicity; NF-κB protein; Nickel; Nickel - toxicity; Oxidative Stress - drug effects; Renal function; Toxicity; transcription factor
• ISSN: 0886-022X; 1525-6049
• DOI: 10.1080/0886022X.2024.2344656

Nickel (Ni) is a common metal with a nephrotoxic effect, damaging the kidneys. This study investigated the mechanism by which gallic acid (GA) protects mice kidneys against renal damage induced by Nickel oxide nanoparticles (NiO-NPs). Forty male Swiss albino mice were randomly assigned into four groups, each consisting of ten mice (  = 10/group): Group I the control group, received no treatment; Group II, the GA group, was administrated GA at a dosage of 110 mg/kg/day body weight; Group III, the NiO-NPs group, received injection of NiO-NPs at a concentration of 20 mg/kg body weight for 10 consecutive days; Group IV, the GA + NiO-NPs group, underwent treatment with both GA and NiO-NPs. The results showed a significant increase in serum biochemical markers and a reduction in antioxidant activities. Moreover, levels of 8-hydroxy-2'-deoxyguanosine (8-OH-dG), phosphorylated nuclear factor kappa B (p65), and protein carbonyl (PC) were significantly elevated in group III compared with group I. Furthermore, the western blot analysis revealed significant high NF-κB p65 expression, immunohistochemistry of the NF-κB and caspase-1 expression levels were significantly increased in group III compared to group I. Additionally, the histopathological inspection of the kidney in group III exhibited a substantial increase in extensive necrosis features compared with group I. In contrast, the concomitant coadministration of GA and NiO-NPs in group IV showed significant biochemical, antioxidant activities, immunohistochemical and histopathological improvements compared with group III. Gallic acid has a protective role against kidney dysfunction and renal damage in Ni-nanoparticle toxicity.