Hypoxic preconditioning attenuates lipopolysaccharide-induced oxidative stress in rat kidneys

被引:32
作者
Yang, Chih-Ching
Ma, Ming-Chieh
Chien, Chiang-Ting
Wu, Ming-Shiou
Sun, Wan-Kuan
Chen, Chau-Fong
机构
[1] Natl Taiwan Univ, Coll Med, Dept Physiol, Taipei 10764, Taiwan
[2] Taipei City Hosp, Heping Branch, Taipei 100, Taiwan
[3] Natl Yang Ming Univ, Fac Med, Sch Med, Taipei 112, Taiwan
[4] Fu Jen Catholic Univ, Sch Med, Hsinchu 242, Taiwan
[5] Natl Taiwan Univ, Natl Taiwan Univ Hosp, Dept Med Res, Taipei 100, Taiwan
[6] Natl Taiwan Univ Hosp, Dept Internal Med, Nephrol Sect, Taipei, Taiwan
来源
JOURNAL OF PHYSIOLOGY-LONDON | 2007年 / 582卷 / 01期
关键词
D O I
10.1113/jphysiol.2006.122747
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Chronic hypoxic (CH) preconditioning reduces superoxide-induced renal dysfunction via the upregulation of superoxide dismutase (SOD) activity and contents. Endotoxaemia reduces renal antioxidant status. We hypothesize that CH preconditioning might protect the kidney from subsequent endotoxaemia-induced oxidative injury. Endotoxaemia was induced by intraperitoneal injection of lipopolysaccharide (LPS; 4 mg kg(-1)) in rats kept at sea level (SL) and rats with CH in an altitude chamber (5500 m for 15 h day(-1)) for 4 weeks. LPS enhanced xanthine oxidase (XO) and gp91phox (catalytic subunit of NADPH oxidase) expression associated with burst amount of superoxide production from the SL kidney surface and renal venous blood detected by lucigenin-enhanced chemiluminescence. LPS induced a morphologic-independent renal dysfunction in baseline and acute saline loading stages and increased renal IL-1 beta protein and urinary protein concentration in the SL rats. After 4 weeks of induction, CH significantly increased Cu/ZnSOD, MnSOD and catalase expression (16 +/- 17, 128 +/- 35 and 48 +/- 21, respectively) in renal cortex, and depressed renal cortex XO (44 +/- 16%) and renal cortex (20 +/- 9%) and medulla (28 +/- 11%) gp91phox when compared with SL rats. The combined effect of enhanced antioxidant proteins and depressed oxidative proteins significantly reduced LPS-enhanced superoxide production, renal XO and gp91phox expression, renal IL-1 beta production, and urinary protein level. CH also ameliorated LPS-induced renal dysfunction in the baseline and acute saline loading periods. We conclude that CH treatment enhances the intrarenal antioxidant/oxidative protein ratio to overcome endotoxaemia-induced reactive oxygen species formation and inflammatory cytokine release.
引用
收藏
页码:407 / 419
页数:13
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