Protective effect of quercetin against renal toxicity induced by cadmium in rats
Balkan Medical Journal, cilt.29, sa.1, ss.56-61, 2012 (SCI-Expanded, Scopus, TRDizin)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 29 Sayı: 1
- Basım Tarihi: 2012
- Doi Numarası: 10.5152/balkanmedj.2011.014
- Dergi Adı: Balkan Medical Journal
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, TR DİZİN (ULAKBİM)
- Sayfa Sayıları: ss.56-61
- Anahtar Kelimeler: Cadmium, Immunohistochemistry, Quercetin, Renal toxicity, TUNEL
- Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
- Trakya Üniversitesi Adresli: Evet
Özet
Objective: The aim of the present study was to examine the protective effect of quercetine (QE) against cadmium (Cd)-induced renal toxicity. Material and Methods: A total of 24 male Wistar albino rats were divided into three groups: control, Cd-treated and Cd-treated with QE; each group containing 8 animals. The Cd-treated group was injected subcutaneously with CdCl2 dissolved in saline in the dose of 2 ml/kg/day for 30 days, resulting in a dosage of 1 mg/kg Cd. The rats in the QE treated groups were given QE (15 mg/kg body weight) once a day intraperitoneally starting 2 days prior to Cd injection during the study period. Results: The renal histology in Cd-treated rats showed mesangial expansion, thickening of capsular basement membranes, glomerular basement membranes and tubular basement membranes, characterized by an increase in periodic acid Schiff (PAS)-positive areas as compared with control animals. With the QE treatment, despite the presence of only a few swollen glomeruli, we noticed a marked protection of renal structure when compared with the Cd-treated rats. Furthermore, QE pretreatment resulted in increased proliferating cell nuclear antigen (PCNA) immunoreactivity and decreased the activity of Terminal Transferase dUTP Nick End Labeling (TUNEL). Conclusion: These findings suggest that QE may attenuate Cd-induced renal toxicity. © Trakya University Faculty of Medicine.