Protective Effects of Quercetin Against HgCl2-Induced Nephrotoxicity in Sprague-Dawley Rats

• Published in: Journal of medicinal food Vol. 18; no. 5; pp. 524 - 534
• Main Authors: Shin, Yu Jin, Kim, Jeong Jun, Kim, Ye Ji, Kim, Won Hee, Park, Eun Young, Kim, In Young, Shin, Han-Seung, Kim, Kyeong Seok, Lee, Eui-Kyung, Chung, Kyu Hyuck, Lee, Byung Mu, Kim, Hyung Sik
• Format: Journal Article
• Language: English
• Published: United States Mary Ann Liebert, Inc 01.05.2015
• Subjects: Acute Kidney Injury - chemically induced; Acute Kidney Injury - drug therapy; Acute Kidney Injury - genetics; Acute Kidney Injury - metabolism; Acute-Phase Proteins - genetics; Acute-Phase Proteins - metabolism; Animals; apoptosis; biomarkers; blood chemistry; blood serum; Cell Adhesion Molecules - genetics; Cell Adhesion Molecules - metabolism; chemokine CCL2; creatinine; excretion; histopathology; Humans; Kidney - drug effects; Kidney - metabolism; kidneys; Lipocalins - genetics; Lipocalins - metabolism; Male; males; medicinal properties; mercuric chloride; Mercuric Chloride - metabolism; Mercuric Chloride - toxicity; mercury; metalloproteinases; metallothionein; nephrotoxicity; neutrophils; oral administration; pollutants; Protective Agents - administration & dosage; protective effect; Proto-Oncogene Proteins - genetics; Proto-Oncogene Proteins - metabolism; quercetin; Quercetin - pharmacology; Rats; Rats, Sprague-Dawley; urea nitrogen; Vascular Endothelial Growth Factor A - genetics; Vascular Endothelial Growth Factor A - metabolism; vascular endothelial growth factors; quercetin; acute kidney injury; metallothionein; protective effect; mercury
• ISSN: 1557-7600; 1557-7600
• DOI: 10.1089/jmf.2014.3242

Mercury is a well-known environmental pollutant that can cause nephropathic diseases, including acute kidney injury (AKI). Although quercetin (QC), a natural flavonoid, has been reported to have medicinal properties, its potential protective effects against mercury-induced AKI have not been evaluated. In this study, the protective effect of QC against mercury-induced AKI was investigated using biochemical parameters, new protein-based urinary biomarkers, and a histopathological approach. A 250 mg/kg dose of QC was administered orally to Sprague-Dawley male rats for 3 days before administration of mercury chloride (HgCl₂). All animals were sacrificed at 24 h after HgCl₂ treatment, and biomarkers associated with nephrotoxicity were measured. Our data showed that QC absolutely prevented HgCl₂-induced AKI, as indicated by biochemical parameters such as blood urea nitrogen (BUN) and serum creatinine (sCr). In particular, QC markedly decreased the accumulation of Hg in the kidney. Urinary excretion of protein-based biomarkers, including clusterin, kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), monocyte chemoattractant protein-1 (MCP-1), tissue inhibitor of metalloproteinases 1 (TIMP-1), and vascular endothelial growth factor (VEGF) in response to HgCl₂ administration were significantly decreased by QC pretreatment relative to that in the HgCl₂-treated group. Furthermore, urinary excretion of metallothionein and Hg were significantly elevated by QC pretreatment. Histopathological examination indicated that QC protected against HgCl₂-induced proximal tubular damage in the kidney. A TUNEL assay indicated that QC pretreatment significantly reduced apoptotic cell death in the kidney. The administration of QC provided significant protective effects against mercury-induced AKI.