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Quercetin Protects against Cadmium-Induced Renal Uric Acid Transport System Alteration and Lipid Metabolism Disorder in Rats.

Wang J, Pan Y, Hong Y, Zhang QY, Wang XN, Kong LD - Evid Based Complement Alternat Med (2012)

Bottom Line: The aim of this study was to determine the effect of quercetin, a dietary flavonoid with anti-hyperuricemic and anti-dyslipidemic properties, on the alteration of renal UA transport system and disorder of renal lipid accumulation in 3 and 6 mg/kg Cd-exposed rats for 4 weeks.We had proved that Cd-induced disorder of renal UA transport and production system might have cross-talking with renal AMPK-PPARα/PGC-1β signal pathway impairment, contributing to Cd nephrotoxicity of rats.Quercetin was found to be effective against Cd-induced dysexpression of RST and OAT1 with XOR hyperactivity and impairment of AMPK-PPARα/PGC-1β signal pathway, resulting in renal lipid accumulation reduction of rats.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210093, China.

ABSTRACT
Hyperuricemia and dyslipidemia are involved in Cd nephrotoxicity. The aim of this study was to determine the effect of quercetin, a dietary flavonoid with anti-hyperuricemic and anti-dyslipidemic properties, on the alteration of renal UA transport system and disorder of renal lipid accumulation in 3 and 6 mg/kg Cd-exposed rats for 4 weeks. Cd exposure induced hyperuricemia with renal XOR hyperactivity and UA excretion dysfunction in rats. Simultaneously, abnormal expression levels of renal UA transport-related proteins including RST, OAT1, MRP4 and ABCG2 were observed in Cd-exposed rats with inhibitory activity of renal Na(+)-K(+)-ATPase. Furthermore, Cd exposure disturbed lipid metabolism with down-regulation of AMPK and its downstream targets PPARα, OCTN2 and CPT1 expressions, and up-regulation of PGC-1β and SREBP-1 expressions in renal cortex of rats. We had proved that Cd-induced disorder of renal UA transport and production system might have cross-talking with renal AMPK-PPARα/PGC-1β signal pathway impairment, contributing to Cd nephrotoxicity of rats. Quercetin was found to be effective against Cd-induced dysexpression of RST and OAT1 with XOR hyperactivity and impairment of AMPK-PPARα/PGC-1β signal pathway, resulting in renal lipid accumulation reduction of rats.

No MeSH data available.


Related in: MedlinePlus

Renal cortex morphology in rats of a 4-week treatment of CdCl2 exposure and coadministration of quercetin. The kidney tissue slices were stained with hematoxylin or oil red O and then observed by microscope (original magnification ×200). Normal rat kidney (a) showed the identical structure of glomerulus and proximal tubules. CdCl2 exposure at 3 mg/kg (b) and 6 mg/kg (c) induced moderate inflammatory infiltration (black arrows). Quercetin at 50 mg/kg (d; f) and 100 mg/kg (e; g) significantly attenuated CdCl2-induced inflammatory infiltration around glomerulus and proximal tubules in kidney of rats. Normal rat kidney (h) showed no lipid deposition. CdCl2 exposure at 3 mg/kg (i) and 6 mg/kg (j) induced moderate lipid deposition (red). Quercetin at 50 mg/kg (k; m) and 100 mg/kg (l; n) significantly attenuated CdCl2-induced renal lipid deposition in renal tubular epithelial cells by oil red O-stain analysis.
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fig3: Renal cortex morphology in rats of a 4-week treatment of CdCl2 exposure and coadministration of quercetin. The kidney tissue slices were stained with hematoxylin or oil red O and then observed by microscope (original magnification ×200). Normal rat kidney (a) showed the identical structure of glomerulus and proximal tubules. CdCl2 exposure at 3 mg/kg (b) and 6 mg/kg (c) induced moderate inflammatory infiltration (black arrows). Quercetin at 50 mg/kg (d; f) and 100 mg/kg (e; g) significantly attenuated CdCl2-induced inflammatory infiltration around glomerulus and proximal tubules in kidney of rats. Normal rat kidney (h) showed no lipid deposition. CdCl2 exposure at 3 mg/kg (i) and 6 mg/kg (j) induced moderate lipid deposition (red). Quercetin at 50 mg/kg (k; m) and 100 mg/kg (l; n) significantly attenuated CdCl2-induced renal lipid deposition in renal tubular epithelial cells by oil red O-stain analysis.

Mentions: Microscopically, 3 and 6 mg/kg Cd-induced mild inflammatory infiltration was observed in renal cortex of rats, which was remarkably ameliorated by the treatment of quercetin (Figures 3(a)–3(f)).


Quercetin Protects against Cadmium-Induced Renal Uric Acid Transport System Alteration and Lipid Metabolism Disorder in Rats.

Wang J, Pan Y, Hong Y, Zhang QY, Wang XN, Kong LD - Evid Based Complement Alternat Med (2012)

Renal cortex morphology in rats of a 4-week treatment of CdCl2 exposure and coadministration of quercetin. The kidney tissue slices were stained with hematoxylin or oil red O and then observed by microscope (original magnification ×200). Normal rat kidney (a) showed the identical structure of glomerulus and proximal tubules. CdCl2 exposure at 3 mg/kg (b) and 6 mg/kg (c) induced moderate inflammatory infiltration (black arrows). Quercetin at 50 mg/kg (d; f) and 100 mg/kg (e; g) significantly attenuated CdCl2-induced inflammatory infiltration around glomerulus and proximal tubules in kidney of rats. Normal rat kidney (h) showed no lipid deposition. CdCl2 exposure at 3 mg/kg (i) and 6 mg/kg (j) induced moderate lipid deposition (red). Quercetin at 50 mg/kg (k; m) and 100 mg/kg (l; n) significantly attenuated CdCl2-induced renal lipid deposition in renal tubular epithelial cells by oil red O-stain analysis.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3368504&req=5

fig3: Renal cortex morphology in rats of a 4-week treatment of CdCl2 exposure and coadministration of quercetin. The kidney tissue slices were stained with hematoxylin or oil red O and then observed by microscope (original magnification ×200). Normal rat kidney (a) showed the identical structure of glomerulus and proximal tubules. CdCl2 exposure at 3 mg/kg (b) and 6 mg/kg (c) induced moderate inflammatory infiltration (black arrows). Quercetin at 50 mg/kg (d; f) and 100 mg/kg (e; g) significantly attenuated CdCl2-induced inflammatory infiltration around glomerulus and proximal tubules in kidney of rats. Normal rat kidney (h) showed no lipid deposition. CdCl2 exposure at 3 mg/kg (i) and 6 mg/kg (j) induced moderate lipid deposition (red). Quercetin at 50 mg/kg (k; m) and 100 mg/kg (l; n) significantly attenuated CdCl2-induced renal lipid deposition in renal tubular epithelial cells by oil red O-stain analysis.
Mentions: Microscopically, 3 and 6 mg/kg Cd-induced mild inflammatory infiltration was observed in renal cortex of rats, which was remarkably ameliorated by the treatment of quercetin (Figures 3(a)–3(f)).

Bottom Line: The aim of this study was to determine the effect of quercetin, a dietary flavonoid with anti-hyperuricemic and anti-dyslipidemic properties, on the alteration of renal UA transport system and disorder of renal lipid accumulation in 3 and 6 mg/kg Cd-exposed rats for 4 weeks.We had proved that Cd-induced disorder of renal UA transport and production system might have cross-talking with renal AMPK-PPARα/PGC-1β signal pathway impairment, contributing to Cd nephrotoxicity of rats.Quercetin was found to be effective against Cd-induced dysexpression of RST and OAT1 with XOR hyperactivity and impairment of AMPK-PPARα/PGC-1β signal pathway, resulting in renal lipid accumulation reduction of rats.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210093, China.

ABSTRACT
Hyperuricemia and dyslipidemia are involved in Cd nephrotoxicity. The aim of this study was to determine the effect of quercetin, a dietary flavonoid with anti-hyperuricemic and anti-dyslipidemic properties, on the alteration of renal UA transport system and disorder of renal lipid accumulation in 3 and 6 mg/kg Cd-exposed rats for 4 weeks. Cd exposure induced hyperuricemia with renal XOR hyperactivity and UA excretion dysfunction in rats. Simultaneously, abnormal expression levels of renal UA transport-related proteins including RST, OAT1, MRP4 and ABCG2 were observed in Cd-exposed rats with inhibitory activity of renal Na(+)-K(+)-ATPase. Furthermore, Cd exposure disturbed lipid metabolism with down-regulation of AMPK and its downstream targets PPARα, OCTN2 and CPT1 expressions, and up-regulation of PGC-1β and SREBP-1 expressions in renal cortex of rats. We had proved that Cd-induced disorder of renal UA transport and production system might have cross-talking with renal AMPK-PPARα/PGC-1β signal pathway impairment, contributing to Cd nephrotoxicity of rats. Quercetin was found to be effective against Cd-induced dysexpression of RST and OAT1 with XOR hyperactivity and impairment of AMPK-PPARα/PGC-1β signal pathway, resulting in renal lipid accumulation reduction of rats.

No MeSH data available.


Related in: MedlinePlus