Effect of ischemia-reperfusion on heat shock protein 70 and 90 gene expression in rat liver - Relation to nutritional status

被引:8
作者
Gasbarrini, A
Esposti, SD
Di Campli, C
De Notariis, S
Loffredo, S
Abraham, A
Simoncini, M
Pola, R
Colantoni, A
Trevisani, F
Bernardi, M
Gasbarrini, G
机构
[1] Univ Cattolica Sacro Cuore, Policlin Gemelli, Ist Patol Med, Dept Internal Med, I-00168 Rome, Italy
[2] Univ Bologna, Dept Internal Med, Bologna, Italy
[3] Brown Univ, Dept Gastroenterol, Providence, RI 02912 USA
关键词
liver; heat shock protein; oxidative stress;
D O I
10.1023/A:1026630706426
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Heat shock proteins are intracellular proteins associated with a generalized response of cells to stress. The purpose of this study was to assess RNA levels of heat shock protein 70 and 90 in fed or fasted rat livers during ischemia-reperfusion. Northern blot analysis of heat shock proteins was performed. Adenosine triphosphate and glutathione were assessed. In baseline conditions, livers of fasted rats showed a twofold increase in mRNA for both heat shock proteins and 38% and 43% reductions in adenosine triphosphate and glutathione, respectively, when compared with organs from fed rats. After ischemia, livers of fasted rats presented a twofold decrease in heat shock protein mRNA, while no changes were observed in livers of fed rats; reduced glutathione and adenosine triphosphate decreased 55% and 50% in fasted livers and 25% and 20% in fed organs, respectively. After 120 min of reperfusion, heat shock protein mRNA rose threefold in fasted livers, while a slight decrease was observed in the fed group; reduced glutathione and adenosine triphosphate returned to 65% and 70% of baseline values in fasted livers and 85% and 90% in fed organs, respectively. In conclusion, the nutritional status affects heat shock protein expression determined by reperfusion. The reduced antioxidant status leading to increased oxidative stress could be the mechanism underlying the phenomenon.
引用
收藏
页码:2601 / 2605
页数:5
相关论文
共 24 条
[1]  
BALKE MJ, 1990, J BIOL CHYEM, V25, P15275
[2]   Early gene response to hepatic ischemia/reperfusion [J].
Broughan, TA ;
Jin, GF ;
Papaconstantinou, J .
JOURNAL OF SURGICAL RESEARCH, 1996, 63 (01) :98-104
[3]  
BUCHMAN TG, 1990, SURGERY, V108, P559
[4]   MULTIPLE MECHANISMS OF IRON-INDUCED FERRITIN SYNTHESIS IN HELA-CELLS [J].
CAIRO, G ;
BARDELLA, L ;
SCHIAFFONATI, L ;
AROSIO, P ;
LEVI, S ;
BERNELLIZAZZERA, A .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1985, 133 (01) :314-321
[5]  
CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1016/0003-2697(87)90021-2
[6]   HEAT-SHOCK RESPONSE AND LIMITATION OF TISSUE NECROSIS DURING OCCLUSION REPERFUSION IN RABBIT HEARTS [J].
CURRIE, RW ;
TANGUAY, RM ;
KINGMA, JG .
CIRCULATION, 1993, 87 (03) :963-971
[7]   REOXYGENATION INJURY IN RAT HEPATOCYTES - MEDIATION BY O2-/H2O2 LIBERATED BY SOURCES OTHER THAN XANTHINE-OXIDASE [J].
DEGROOT, H ;
BRECHT, M .
BIOLOGICAL CHEMISTRY HOPPE-SEYLER, 1991, 372 (01) :35-41
[8]   HEAT-SHOCK PROTEIN INDUCTION IN RAT HEARTS - A ROLE FOR IMPROVED MYOCARDIAL SALVAGE AFTER ISCHEMIA AND REPERFUSION [J].
DONNELLY, TJ ;
SIEVERS, RE ;
VISSERN, FLJ ;
WELCH, WJ ;
WOLFE, CL .
CIRCULATION, 1992, 85 (02) :769-778
[9]  
GASBARRINI A, 1992, J BIOL CHEM, V267, P6654
[10]  
GASBARRINI A, 1994, TRANSPL P, V26, P3408