Curcumin ameliorates cadmium-induced nephrotoxicity in Sprague-Dawley rats

Food Chem Toxicol. 2018 Apr:114:34-40. doi: 10.1016/j.fct.2018.02.007. Epub 2018 Feb 6.

Abstract

Chronic exposure to cadmium (Cd) causes remarkable damage to the kidneys, a target organ of accumulated Cd after oral administration. The aim of the present study was to investigate the protective effect of curcumin against Cd-induced nephrotoxicity. Sprague-Dawley male rats were divided into the following four treatment groups: control, curcumin (50 mg/kg, oral), CdCl2, (25 mg/kg, oral), and pre-treatment with curcumin (50 mg/kg) 1 h prior to the administration of CdCl2 (25 mg/kg, oral) for 7 days. At 24 h after the final treatment, the animals were killed, and the biomarkers associated with nephrotoxicity were measured. Our data indicated that blood urea nitrogen (BUN) and serum creatinine (sCr) levels were significantly reduced by curcumin pre-treatment in CdCl2-treated animals. Histopathological studies showed hydropic swelling and hypertrophy of the proximal tubular cells in the renal cortex after Cd treatment. Pretreatment with curcumin ameliorated the histological alterations induced by Cd. The urinary excretion of kidney injury molecule-1 (Kim-1), osteopontin (OPN), tissue inhibitor of metalloproteinases 1 (TIMP-1), neutrophil gelatinase-associated lipocalin (NGAL), and netrin-1 significantly reduced by curcumin treatment compared to that in the CdCl2-treated group. The administration of curcumin provided a significant protective effect against Cd-induced nephrotoxicity.

Keywords: Cadmium; Curcumin; Renal toxicity; Urinary biomarker.

MeSH terms

  • Acute Kidney Injury / drug therapy*
  • Acute Kidney Injury / etiology
  • Acute Kidney Injury / metabolism
  • Acute Kidney Injury / physiopathology
  • Animals
  • Apoptosis / drug effects
  • Cadmium / toxicity*
  • Curcumin / administration & dosage*
  • Hepatitis A Virus Cellular Receptor 1 / genetics
  • Hepatitis A Virus Cellular Receptor 1 / metabolism
  • Humans
  • Kidney / drug effects
  • Kidney / metabolism
  • Kidney / physiopathology
  • Male
  • Osteopontin / genetics
  • Osteopontin / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Tissue Inhibitor of Metalloproteinase-1 / genetics
  • Tissue Inhibitor of Metalloproteinase-1 / metabolism

Substances

  • Havcr1 protein, mouse
  • Hepatitis A Virus Cellular Receptor 1
  • Tissue Inhibitor of Metalloproteinase-1
  • Cadmium
  • Osteopontin
  • Curcumin