The expression of cyclooxygenases and lipoxygenases in renal ischemia-reperfusion injury

被引:25
作者
Matsuyama, M
Nakatani, T
Hase, T
Kawahito, Y
Sano, H
Kawamura, M
Yoshimura, R
机构
[1] Osaka City Univ, Grad Sch Med, Dept Urol, Abeno Ku, Osaka 5458585, Japan
[2] Kyoto Prefectural Univ Med, Dept Internal Med 1, Kyoto 602, Japan
[3] Hyogo Med Univ, Dept Internal Med, Nishinomiya, Hyogo, Japan
关键词
D O I
10.1016/j.transproceed.2004.08.054
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Recent studies of ischemia-reperfusion (I/R) injury have focused on the function of neutrophils as well as the actions of inflammatory cytokines. However, few reports address cyclooxygenases (COXs) and lipoxygenases (LOXs). We researched the expression of COXs (COX-1 and COX-2) and LOXs (5-LOX and 12-LOX) in rat renal I/R injury. The right kidney of male Lewis rats was excised, and the left renal artery and vein clamped for a 90-minute ischemia time. Rats were humanely killed at 0, 1.5, 3, 5, and 12 hours after reperfusion. COX and LOX expressions were studied using immunohistostaining. COX-2 and LOX expressions were observed only on endothelial cells of normal kidney. From 1.5 A to 5 hours after reperfusion, COX-2 and LOXs expressions gradually intensified on endothelial cells. COX-2 and LOXs expression were most intense on endothelial cells at 5 hours after reperfusion. Twelve hours after reperfusion, necrosis extended throughout the ischemic kidney and nearly all the tubular epithelial cells were destroyed. Thus, at 12 hours after reperfusion, COX-2 and LOXs expressions on endothelial cells became weaker. However, COX-1 expression was not different at every time after reperfusion. A COX-2 and LOXs were expressed in a rat model showing renal I/R injury. Several hours after the maximum of COX-2 and LOXs expressions, the maximal renal I/R injury was observed. These results suggest a relationship between COX-2 and LOXs expressions and renal I/R injury.
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页码:1939 / 1942
页数:4
相关论文
共 23 条
[1]   Lipoxygenases: Occurrence, functions, catalysis, and acquisition of substrate [J].
Brash, AR .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (34) :23679-23682
[2]   ENDOTOXIN-INDUCED LUNG INJURY IN RATS - ROLE OF EICOSANOIDS [J].
CHANG, SW ;
WESTCOTT, JY ;
PICKETT, WC ;
MURPHY, RC ;
VOELKEL, NF .
JOURNAL OF APPLIED PHYSIOLOGY, 1989, 66 (05) :2407-2418
[3]   In vivo correlation of neutrophil receptor expression, ischemia-reperfusion injury, and selective 5-lipoxygenase inhibition in guinea pigs [J].
Dolan, R ;
Hartshorn, K ;
Andry, C ;
Tablante, J ;
Grillone, G ;
McAvoy, D ;
Suntra, C .
ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY, 1998, 124 (12) :1377-1380
[4]   Inhibition of intercellular adhesion molecule-1 with antisense deoxynucleotides prolongs renal isograft survival in the rat [J].
Dragun, D ;
Lukitsch, I ;
Tullius, SG ;
Qun, Y ;
Park, JK ;
Schneider, W ;
Luft, FC ;
Haller, H .
KIDNEY INTERNATIONAL, 1998, 54 (06) :2113-2122
[5]  
FUNK CD, 1996, BIOCHIM BIOPHYS ACTA, V11, P65
[6]   Cyclooxygenase-1 and-2 in human testicular tumours [J].
Hase, T ;
Yoshimura, R ;
Matsuyama, M ;
Kawahito, Y ;
Wada, S ;
Tsuchida, K ;
Sano, H ;
Nakatani, T .
EUROPEAN JOURNAL OF CANCER, 2003, 39 (14) :2043-2049
[7]  
HASHIMOTO H, 1990, ARZNEIMITTEL-FORSCH, V40-1, P126
[8]   Levels of cyclooxygenase-1 and -2 mRNA expression at various stages of acute gastric injury induced by ischemia-reperfusion in rats [J].
Kishimoto, Y ;
Wada, K ;
Nakamoto, K ;
Kawasaki, H ;
Hasegawa, J .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1998, 352 (01) :153-157
[9]   Selective cyclo-oxygenase-2 inhibitors aggravate ischaemia-reperfusion injury in the rat stomach [J].
Maricic, N ;
Ehrlich, K ;
Gretzer, B ;
Schuligoi, R ;
Respondek, M ;
Peskar, BM .
BRITISH JOURNAL OF PHARMACOLOGY, 1999, 128 (08) :1659-1666
[10]  
Matsuyama M, 2004, INT J ONCOL, V24, P821