Macedo Francisco Yuri Bulcão, Baltazar Fátima, Mourão Lívia Cajaseiras, Almeida Paulo Roberto Carvalho, Mota José Mauricio S C, Schmitt Fernando C, Ribeiro Ronaldo A
Department of Physiology and Pharmacology, Federal University of Ceara, Rua Coronel Nunes de Melo, 1315, Rodolfo Teofilo, 60430-270 fortaleza, CE, Brazil.
Exp Toxicol Pathol. 2008 Apr;59(6):425-30. doi: 10.1016/j.etp.2007.10.010. Epub 2008 Jan 29.
Acrolein (ACR) is a urinary metabolite of cyclophosphamide (CPS) and ifosfamide (IFS), which has been demonstrated to be the causative agent of hemorrhagic cystitis (HC), induced by these compounds. In this study, we investigate the participation of cyclooxygenase-2 (COX-2) on ACR-induced HC.
Male Wistar rats (150-200g; 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.
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.
COX-2 participates in the pathogenesis of ACR-induced HC first seen 12h after initial contact between ACR and urothelium.
丙烯醛（ACR）是环磷酰胺（CPS）和异环磷酰胺（IFS）的尿液代谢产物，已被证明是这些化合物诱导的出血性膀胱炎（HC）的致病因子。在本研究中，我们调查了环氧合酶-2（COX-2）在ACR诱导的HC中的作用。
雄性Wistar大鼠（150-200g；每组6只大鼠）用蒸馏水或膀胱内注射ACR处理，并通过膀胱湿重、宏观和微观参数以及COX-2表达的变化进行分析。
ACR给药12小时后，COX-2免疫组化表达显著，主要位于上皮下细胞。根据Gray标准分析，ACR注射还改变了大鼠膀胱的一些宏观和微观参数。
COX-2参与了ACR诱导的HC的发病机制，在ACR与尿路上皮首次接触后12小时首次出现。
