Cannabidiol treatment ameliorates ischemia/reperfusion renal injury in rats

被引：32
作者：
Fouad, Amr A. [1 ]
Al-Mulhim, Abdulruhman S. [2 ]
Jresat, Iyad [3 ]
机构：
[1] King Faisal Univ, Coll Med, Dept Biomed Sci, Div Pharmacol, Al Hasa 31982, Saudi Arabia
[2] King Faisal Univ, Coll Med, Dept Surg, Al Hasa 31982, Saudi Arabia
[3] King Faisal Univ, Coll Med, Dept Biomed Sci, Div Pathol, Al Hasa 31982, Saudi Arabia
来源：
LIFE SCIENCES | 2012年 / 91卷 / 7-8期
关键词：
Cannabidiol; Ischemia/reperfusion; Kidney; Oxidative stress; Inflammation; ISCHEMIA-REPERFUSION INJURY; CHRONIC KIDNEY-DISEASE; OXIDATIVE STRESS; KAPPA-B; SURVIVIN; INFLAMMATION; CONSTITUENT; DYSFUNCTION; GENERATION; INHIBITOR;
D O I：
10.1016/j.lfs.2012.07.030
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
Aims: To investigate the protective effect of cannabidiol, the major non-psychotropic Cannabis constituent, against renal ischemia/reperfusion injury in rats. Main methods: Bilateral renal ischemia was induced for 30 min followed by reperfusion for 24 h. Cannabidiol (5 mg/kg, i.v.) was given 1 h before and 12 h following the procedure. Key findings: Ischemia/reperfusion caused significant elevations of serum creatinine and renal malondialdehyde and nitric oxide levels, associated with a significant decrease in renal reduced glutathione. Cannabidiol significantly attenuated the deterioration in the measured biochemical parameters induced by ischemia/reperfusion. Histopathological examination showed that cannabidiol ameliorated ischemia/reperfusion-induced kidney damage. Immunohistochemical analysis revealed that cannabidiol significantly reduced the expression of inducible nitric oxide synthase, tumor necrosis factor-alpha, cyclooxygenase-2, nuclear factor-kappa B, Fas ligand and caspase-3, and increased the expression of survivin in ischemic/reperfused kidney tissue. Significance: Cannabidiol, via its antioxidant and anti-inflammatory properties, may represent a potential therapeutic option to protect against ischemia/reperfusion renal injury. (C) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码：284 / 292
页数：9
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