Protection of endotoxin-incluced oxidative renal tissue damage of rats by vitamin E or/and EGb 761 treatment


Coskun O., Armutcu F., Kanter M., Kuzey G.

JOURNAL OF APPLIED TOXICOLOGY, cilt.25, ss.8-12, 2005 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 25 Konu: 1
  • Basım Tarihi: 2005
  • Doi Numarası: 10.1002/jat.1002
  • Dergi Adı: JOURNAL OF APPLIED TOXICOLOGY
  • Sayfa Sayıları: ss.8-12

Özet

The aim of the present study was to evaluate the possible protective effects of vitamin E and EGb 761 treatments, alone or in combination, against oxidative renal tissue damage in experimentally induced endotoxaemic rats. Fifty healthy male Wistar albino rats, weighing 150-250 g and averaging 12 weeks old, were allotted randomly into one of five experimental groups: A (untreated), B (endotoxaemic), C (endotoxaemic + vitamin E treated), D (endotoaxemic + EGb 761 treated) and E (endotoxaemic + vitamin E and EGb 761 treated), each containing ten animals. Group A received only an intraperitoneal (i.p.) injection of 2 ml of normal saline solution and served as the control. Groups B, C, D and E were administrated a single i.p. injection of 0.5 ml of endotoxin solution. In addition, groups C, D and E received i.p. injections of 600 mg kg(-1) body mt. of vitamin E and oral extract of 50 mg kg(-1) body wt. of EGb 761, alone or in combination, immediately after the endotoxin injection. The experiment lasted for 24 h. At the end of the experiment blood and tissue samples were obtained for biochemical and histopathological investigation. Endotoxin injection produced renal damage, increased lipid peroxidation and decreased antioxidant enzyme activity. Vitamin E or/and EGb 761 treatment decreased lipid peroxidation, increased antioxidant enzyme activity and also prevented renal tissue damage in experimentally induced endotoxaemic rats. In conclusion, vitamin E and EGb 761 treatment, alone or in combination, appears to be beneficial in preventing endotoxin-induced oxidative renal tissue damage and therefore shows potential for clinical use. Copyright (C) 2005 John Wiley Sons, Ltd.