Troxerutin protects the mouse kidney from D-galactose-caused injury through anti-inflammation and anti-oxidation

被引:122
作者
Fan, Shao-hua [1 ]
Zhang, Zi-feng [1 ]
Zheng, Yuan-lin [1 ]
Lu, Jun [1 ]
Wu, Dong-mei [1 ]
Shan, Qun [1 ]
Hu, Bin [1 ]
Wang, Yan-yan [2 ]
机构
[1] Xuzhou Normal Univ, Sch Life Sci, Key Lab Biotechnol Med Plants Jiangsu Prov, Xuzhou 221116, Peoples R China
[2] First Renmin Hosp Xuzhou, Dept Oncol, Xuzhou 221002, Peoples R China
关键词
Troxerutin; D-galactose; Antioxidant enzyme; NF-kappa B; COX-2; iNOS; EP2; PROSTAGLANDIN E-2; OXIDATIVE STRESS; RECEPTORS EP2; NITRIC-OXIDE; EXPRESSION; MACROPHAGES; COX-2; INHIBITION; DAMAGE; ACID;
D O I
10.1016/j.intimp.2008.10.008
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
This study was carried out to investigate the protective effect of troxerutin against D-galactose (D-gal)induced renal injury in mice. Hematoxylin and eosin (H&E) stained sections of kidneys revealedD-gal could cause renal injury and troxerutin Could significantly attenuate the injury. We further investigated the mechanisms involved in the protective effects of troxerutin on mouse kidney. The following antioxidant defense enzymes were measured: cytosolic Cu/Zn superoxide dismutase (SOD-1), catalase (CAT) and glutathione peroxidase (GPx). The content of the lipid peroxidation product malondialdehyde (MDA) was also analyzed. In D-gal-treated mice, antioxidant enzymes activities were significantly decreased and the level of MDA was significantly higher than those in the vehicle controls. Our results indicated that the protective effect of troxerutin against D-gal induced renal injury might be caused, at least in part, by increasing the activity of antioxidant enzymes with a reduction in lipid peroxidation product. Furthermore, we also examined the inflammatory signal mediators of nuclear factor-kappa B (NF-kappa B), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and prostanoid receptor Subtype EP2 by Western blot. After treatment with D-gal, the NF-kappa B p65, iNOS, COX-2 and EP2 were markedly upregulated. Upon co-treatment with the troxerutin, however, the expressions of the NF-kappa B p65, iNOS, COX-2 and EP2 markedly reduced, compared to D-gal treatment alone. These results indicated that troxerutin has significantly inhibitory effects on the NF-kappa B-mediated inflammatory response. These findings suggest troxerutin Could attenuate renal injury induced by D-gal probably through its antioxidant and anti-inflammation properties. Crown Copyright (C) 2008 Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:91 / 96
页数:6
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