Evaluation of Smilax excelsa L. Use in Experimentally Induced Nephrotoxicity


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Ozsoy N., Okyar A., Arda-Pirincci P., Can A., Bolkent S., Akev N.

KAFKAS UNIVERSITESI VETERINER FAKULTESI DERGISI, cilt.19, ss.807-814, 2013 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 19
  • Basım Tarihi: 2013
  • Doi Numarası: 10.9775/kvfd.2013.9253
  • Dergi Adı: KAFKAS UNIVERSITESI VETERINER FAKULTESI DERGISI
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, TR DİZİN (ULAKBİM)
  • Sayfa Sayıları: ss.807-814
  • Anahtar Kelimeler: Smilax excelsa, Renal damage, Carbon tetrachloride, Antioxidant effect, Nephrotoxicity, ANTIOXIDANT ACTIVITY, HYDROGEN-PEROXIDE, CHINA LINN., GLUTATHIONE, CELL, FLAVONOIDS, CAPACITY, EXTRACTS, SAPONINS, GLABRAE
  • İstanbul Üniversitesi Adresli: Evet

Özet

The protective effect of an aqueous extract of the shoots and leaves of Smilax excelsa L. against acute carbon tetrachloride (CCl4)induced toxicity and the changes in antioxidative defense activities in kidney of rats were investigated. Female Wistar rats were supplied with S. excelsa shoots and leaves aqueous extract once a day for 9 days (orally at a dose of 100, 200 and 400 mg/kg of body weight) prior to renal injury induction through intraperitoneal injection with a single dose of CCl4 (1 ml/kg body wt, in a 20 % v/v olive oil solution) on the 10th day. 24 h after CCl4 intoxication serum and tissue biochemical and hispathological analyses were undertaken after sacrification under anesthesia. Administration of the extract reversed the antioxidant parameters which were impaired in CCl4 group, in a dose dependent manner and at a dose of 400 mg/kg of body weight the levels of almost all the parameters were almost back to normal Control group. Nevertheless, the extract did not completely improve the CCl4-induced degenerative changes observed microscopically in kidney tissue. The results of this study suggest that S. excelsa could protect the kidney tissue against CCl4-induced nephrotoxicity in rats, probably by increasing antioxidative defense activities.