Glucocorticoid pretreatment protects cardiac function and induces cardiac heat shock protein 72

被引:58
作者
Valen, G [1 ]
Kawakami, T
Tähepôld, P
Dumitrescu, A
Löwbeer, C
Vaage, J
机构
[1] Karolinska Hosp, Crafoord Lab Expt Surg L6 00, S-17176 Stockholm, Sweden
[2] Karolinska Hosp, Dept Thorac Surg, S-17176 Stockholm, Sweden
[3] Huddinge Univ Hosp, Dept Clin Chem, S-14186 Huddinge, Sweden
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 2000年 / 279卷 / 02期
关键词
methylprednisolone; dexamethasone; hydrocortisone; ischemia-reperfusion;
D O I
10.1152/ajpheart.2000.279.2.H836
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Acute administration of glucocortiocoids reduces inflammation. Increasing knowledge of the mechanisms of action indicate that pretreatment with glucocorticoids could have organ-protective effects. We investigated whether pretreatment with methylprednisolone (MP) protected the heart against ischemia-reperfusion dysfunction, and we hypothetized that this protection might be due to induction of the cardioprotective heat shock protein 72 (HSP72). Rats were given vehicle or MP-40 mg/kg im as a double injection starting either 24 or 120 h (5 days) before their hearts were excised for Langendorff perfusion (n = 6-11 hearts in each group). MP improved left ventricular function and coronary flow during reperfusion after 30 min of global ischemia and reduced infarct size. Cardiac HSP72 gradually increased in a 24-h time course after MP treatment, and the increase was sustained 5 days afterward (immunoblotting). HSP72 mRNA was either reduced or unchanged, indicating a posttranscriptional regulation. Pretreatment with hydrocortisone or dexamethasone (n = 7-8 hearts of each) similarily increased cardiac HSP72 24 h afterward. This paper demonstrates that glucocorticoids increase cardiac HSP72 and protect organ function against ischemia-reperfusion injury.
引用
收藏
页码:H836 / H843
页数:8
相关论文
共 23 条
[11]   Heat shock response - Pathophysiological implications [J].
Leppa, S ;
Sistonen, L .
ANNALS OF MEDICINE, 1997, 29 (01) :73-78
[12]   METHYLPREDNISOLONE NORMALIZES SUPEROXIDE ANION PRODUCTION BY POLYMORPHS FROM PATIENTS WITH ANCA-POSITIVE VASCULITIDES [J].
MACCONI, D ;
ZANOLI, AF ;
ORISIO, S ;
LONGARETTI, L ;
MAGRINI, L ;
ROTA, S ;
RADICE, A ;
POZZI, C ;
REMUZZI, G .
KIDNEY INTERNATIONAL, 1993, 44 (01) :215-220
[13]   OVEREXPRESSION OF THE RAT INDUCIBLE 70-KD HEAT-STRESS PROTEIN IN A TRANSGENIC MOUSE INCREASES THE RESISTANCE OF THE HEART TO ISCHEMIC-INJURY [J].
MARBER, MS ;
MESTRIL, R ;
CHI, SH ;
SAYEN, MR ;
YELLON, DM ;
DILLMANN, WH .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 95 (04) :1446-1456
[14]   CARDIAC STRESS PROTEIN ELEVATION 24 HOURS AFTER BRIEF ISCHEMIA OR HEAT-STRESS IS ASSOCIATED WITH RESISTANCE TO MYOCARDIAL-INFARCTION [J].
MARBER, MS ;
LATCHMAN, DS ;
WALKER, JM ;
YELLON, DM .
CIRCULATION, 1993, 88 (03) :1264-1272
[15]  
Morimoto RI, 1997, ESSAYS BIOCHEM, V32, P17
[16]   TRANSGENIC MICE EXPRESSING THE HUMAN HEAT-SHOCK PROTEIN-70 HAVE IMPROVED POSTISCHEMIC MYOCARDIAL RECOVERY [J].
PLUMIER, JCL ;
ROSS, BM ;
CURRIE, RW ;
ANGELIDIS, CE ;
KAZLARIS, H ;
KOLLIAS, G ;
PAGOULATOS, GN .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 95 (04) :1854-1860
[17]   Suppression of NF-κB and AP-1 activation by glucocorticoids in experimental glomerulonephritis in rats:: molecular mechanisms of anti-nephritic action [J].
Sakurai, H ;
Shigemori, N ;
Hisada, Y ;
Ishizuka, T ;
Kawashima, K ;
Sugita, T .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 1997, 1362 (2-3) :252-262
[18]   LATE PRECONDITIONING AGAINST MYOCARDIAL STUNNING - AN ENDOGENOUS PROTECTIVE MECHANISM THAT CONFERS RESISTANCE TO POSTISCHEMIC DYSFUNCTION 24-H AFTER BRIEF ISCHEMIA IN CONSCIOUS PIGS [J].
SUN, JZ ;
TANG, XL ;
KNOWLTON, AA ;
PARK, SW ;
QIU, YM ;
BOLLI, R .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 95 (01) :388-403
[19]   STEROID INHIBITION OF CYTOKINE-MEDIATED VASODILATION AFTER WARM HEART-SURGERY [J].
TEOH, KHT ;
BRADLEY, CA ;
GAULDIE, J ;
BURROWS, H .
CIRCULATION, 1995, 92 (09) :347-353
[20]   Dexamethasone protection of rat intestinal epithelial cells against oxidant injury is mediated by induction of heat shock protein 72 [J].
Urayama, S ;
Musch, MW ;
Retsky, J ;
Madonna, MB ;
Straus, D ;
Chang, EB .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 102 (10) :1860-1865