Induction of COX-2 expression by acrolein in the rat model of hemorrhagic cystitis

被引:11
作者
Bulcao Macedo, Francisco Yuri [1 ]
Baltazar, Fatima [2 ]
Mourao, Livia Cajaseiras [1 ]
Carvalho Almeida, Paulo Roberto [3 ]
Mota, Jose Mauricio S. C. [1 ]
Schmitt, Fernando C. [4 ]
Ribeiro, Ronaldo A. [1 ,5 ]
机构
[1] Univ Fed Ceara, Fac Med, Dept Physiol & Pharmacol, BR-60430270 Fortaleza, Ceara, Brazil
[2] Univ Minho, Sch Hlth Sci, Life & Hlth Sci Res Inst, ICVS, P-4719 Braga, Portugal
[3] Univ Fed Ceara, Fac Med, Dept Pathol, BR-60430270 Fortaleza, Ceara, Brazil
[4] Univ Porto, Inst Mol Pathol & Immunol, IPATIMUP, Oporto, Portugal
[5] Canc Inst Ceara, Dept Clin Oncol, Fortaleza, Ceara, Brazil
关键词
acrolein; hemorrhagic cystitis; cyclooxygenase-2;
D O I
10.1016/j.etp.2007.10.010
中图分类号
R36 [病理学];
学科分类号
100104 [病理学与病理生理学];
摘要
Aim: Acrolein (ACR) is a urinary metabolite of cyclophosphamide (CPS) and ifosfamide (IFS), which has been demonstrated to be the causative agent of hemorrhagic cystitis (HQ, induced by these compounds. In this study, we investigate the participation of cyclooxygenase-2 (COX-2) on ACR-induced HC. Methods: Male Wistar rats (150-200 g; six rats per group) were treated with distilled water or intravesical ACR and analyzed by changes in bladder wet weight, macroscopic and microscopic parameters and COX-2 expression. Results: COX-2 immunohistochemical expression was significant 12h after ACR administration mainly in subepithelial cells. ACR injection also alters some macroscopic and microscopic parameters in bladder of rats analyzed by Gray's criteria. Conclusions: COX-2 participates in the pathogenesis of ACR-induced HC first seen 12 h after initial contact between ACR and urothelium. (c) 2007 Elsevier GmbH. All rights reserved.
引用
收藏
页码:425 / 430
页数:6
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