Quercetin ameliorates methotrexate-induced renal damage, apoptosis and oxidative stress in rats.
BACKGROUND
In the present study, the protective and therapeutic effects of quercetin (QE) on renal injury induced by methotrexate (MTX) have been examined.


METHODS
A total of 24 male rats were divided into the following three groups: control group, MTX group, and MTX + QE group. Rats in MTX group received 20 mg/kg of single dose of MTX, while those in MTX + QE group received 20 mg/kg of single dose MTX, in addition to 15 mg/kg of QE administered 30 min prior to MTX and in the following 5-day period as a single daily dose. At the end of the experimental period, renal tissues were removed for histopathological and biochemical assessments.


RESULTS
Light microscopic examination showed a disruption of the renal structure in rats in MTX group in the form of tubular degeneration and dilation, with shedding of the tubular epithelial cells into the lumen. QE treatment was associated with less marked degenerative changes, with a similar histological appearance to that of controls. Furthermore, QE treatment resulted in decreased the number of apoptotic cells. Biochemical assessments showed significantly higher malondialdehyde (MDA) levels in MTX group as compared to control and MTX + QE groups. superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) levels showed a significant decrease in MTX group as compared to controls. However, QE significantly suppressed MDA level, compensated deficits in the anti-oxidant defenses [reduced SOD, GSH-Px, and CAT levels] in kidney tissue resulted from MTX administration.


CONCLUSIONS
In conclusion, renal toxic effects of MTX may be alleviated by QE.
a Department of Histology and Embryology , Faculty of Medicine, University of Namik Kemal , Tekirdag , Turkey and.
Mustafa
M
Erboga
a Department of Histology and Embryology , Faculty of Medicine, University of Namik Kemal , Tekirdag , Turkey and.
Cevat
C
Aktas
a Department of Histology and Embryology , Faculty of Medicine, University of Namik Kemal , Tekirdag , Turkey and.
Zeynep Fidanol
ZF
Erboga
a Department of Histology and Embryology , Faculty of Medicine, University of Namik Kemal , Tekirdag , Turkey and.
Yeliz Bozdemir
YB
Donmez
b Department of Biochemistry , Faculty of Medicine, University of Namik Kemal , Tekirdag , Turkey.
Ahmet
A
Gurel
D058186:Acute Kidney Injury / Q000139:chemically induced*; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage*; D017209:Apoptosis / Q000187:drug effects*; D002374:Catalase / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008727:Methotrexate / Q000009:adverse effects*; D018384:Oxidative Stress / Q000187:drug effects*; D011794:Quercetin / Q000008:administration & dosage*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism
D000975:Antioxidants; D008315:Malondialdehyde; D011794:Quercetin; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D008727:Methotrexate
Apoptosis; methotrexate; nephrotoxicity; oxidative stress; quercetin