Protective effects of oral Arabic gum administration on gentamicin-induced nephrotoxicity in rats

被引:123
|
作者
Al-Majed, AA
Mostafa, AM
Al-Rikabi, AC
Al-Shabanah, OA
机构
[1] King Saud Univ, Coll Pharm, Dept Pharmacol, Riyadh 11451, Saudi Arabia
[2] King Saud Univ, Coll Med, Dept Pathol, Riyadh 11451, Saudi Arabia
关键词
arabic gum; nephrotoxicity; gentamicin; lipid peroxidation; rat;
D O I
10.1016/S1043661802001251
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Arabic gum (AG) is a complex polysaccharide used as suspending agent. It has been widely used by eastern folk medicine practitioners as a restorative agent and is thought to be an excellent curative for renal failure patients. We therefore tested these folkloric claims using a rat model of gentamicin (GM)-induced nephrotoxicity. AG (7.5 g 100 ml(-1), in drinking water) was administered orally for 8 days concurrently with GM (80 mg kg(-1) per day, i.p.). Estimation of urine volume, serum creatinine and urea concentrations, kidney tissue malondialdehyde (MDA) contents and glutathione (GSH) were carried out after the last dose of GM. Kidneys were also examined for histological changes. GM caused a marked nephrotoxicity as evidenced by significant increases in urine volume (295%), serum creatinine (318%) and urea (258%) and a significant decrease in creatinine clearance (Ccr) (26%). Treatment with AG protected the rats from GM-induced nephrotoxicity as evident by normalisation of these parameters. In addition there was about 187% increase in kidney tissue MDA contents above the control with GM treatment. AG totally prevented the GM-induced rise in kidney tissue contents of MDA. Kidney histology of the tissue from GM-treated rats showed necrosis and desquamation of tubular epithelial cells in renal cortex as well as interstitial nephritis. Whereas it was very much comparable to control when AG was co-administered with GM. In conclusion, AG protected the rats from GM-induced nephrotoxicity, possibly, at least in part through inhibition of the production of oxygen free radicals that cause lipid peroxidation. (C) 2002 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:445 / 451
页数:7
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