Arginine-supplemented diet decreases expression of inflammatory cytokines and improves survival in burned rats

被引:48
作者
Cui, XL [1 ]
Iwasa, M [1 ]
Iwasa, Y [1 ]
Ogoshi, S [1 ]
机构
[1] Kochi Med Sch, Dept Surg 2, Nanko Ku, Kochi 7838505, Japan
关键词
D O I
10.1177/014860710002400289
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Background: We examined whether the expression of inflammatory cytokines in organs was influenced by the enteral diet supplemented with arginine in burned rats. Methods: Male Wistar rats weighing about 200 g underwent catheter jejunostomy and received scald burns covering 30% of the whole-body surface area. Animals were divided into two groups: a control group (no supplemental arginine, n = 12) and an arginine group (supplemental arginine: 7.7 g/L, n = 10), which continuously received total enteral nutrition for 7 days (250 kcal/kg/d, 1.72 gN/kg/d). The following were measured after the experiment: (1) messenger RNA (mRNA) expression of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin-1beta (IL-1 beta), and IL-6 in the spleen, thymus, lung, and liver by a semiquantitative reverse transcription-polymerase chain reaction method, (2) inflammatory cytokines in the plasma and supernatant of cultured splenic lymphocytes by enzyme-linked immunosorbant assay, (3) nitric oxide (NO) product, NO2-/NO3-, in the plasma and supernatant of cultured splenic lymphocytes by the Griess method, and (4) survival rate by the Kaplan-Meier method. Results: The mRNA expression of TNF-alpha was significantly decreased in the spleen and lung (p < .01, p < .05), IFN-gamma in the lung (p < .05), IL-1 beta in the spleen (p < .05), and IL-6 in the thymus and liver (p < .05, p < .05) in the arginine group when compared with the control group. The production of TNF-alpha by splenic lymphocytes was suppressed in the arginine group in both concanavalin A (Con A)-treated and -untreated cultures (p < .01, p < .05). The production of IFN-gamma by splenic lymphocytes treated with Con A was suppressed in the arginine group (p < .05). The NO product in the supernatant without Con A was increased in the arginine group (p < .05). The mortality rate of the arginine group (0%) was lower than that in the control group (33.3%) on day 7 after the burn injury (p < .05). Conclusions: The data suggest that dietary arginine supplementation decreases the mRNA expression of inflammatory cytokines in organs and improves the survival rate after thermal injury.
引用
收藏
页码:89 / 96
页数:8
相关论文
共 34 条
[1]  
ADJEI AA, 1995, NUTRITION, V11, P371
[3]   UREA CYCLE INTERMEDIATE KINETICS AND NITRATE EXCRETION AT NORMAL AND THERAPEUTIC INTAKES OF ARGININE IN HUMANS [J].
BEAUMIER, L ;
CASTILLO, L ;
AJAMI, AM ;
YOUNG, VR .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 1995, 269 (05) :E884-E896
[4]   BENEFICIAL ACTIONS OF S-NITROSO-N-ACETYLPENICILLAMINE, A NITRIC-OXIDE DONOR, IN MURINE TRAUMATIC SHOCK [J].
CHRISTOPHER, TA ;
MA, XL ;
LEFER, AM .
SHOCK, 1994, 1 (01) :19-24
[5]  
DANAS P, 1989, CRIT CARE MED, V17, P975
[6]   CYTOKINE RESPONSE TO BURN INJURY - RELATIONSHIP WITH PROTEIN-METABOLISM [J].
DEBANDT, JP ;
CHOLLETMARTIN, S ;
HERNVANN, A ;
LIORET, N ;
DUROURE, LD ;
LIM, SK ;
VAUBOURDOLLE, M ;
GUECHOT, J ;
SAIZY, R ;
GIBOUDEAU, J ;
CYNOBER, L .
JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE, 1994, 36 (05) :624-628
[7]   THE PROINFLAMMATORY CYTOKINES INTERLEUKIN-1 AND TUMOR-NECROSIS-FACTOR AND TREATMENT OF THE SEPTIC SHOCK SYNDROME [J].
DINARELLO, CA .
JOURNAL OF INFECTIOUS DISEASES, 1991, 163 (06) :1177-1184
[8]   INITIAL EVALUATION OF HUMAN RECOMBINANT INTERLEUKIN-1 RECEPTOR ANTAGONIST IN THE TREATMENT OF SEPSIS SYNDROME - A RANDOMIZED, OPEN-LABEL, PLACEBO-CONTROLLED MULTICENTER TRIAL [J].
FISHER, CJ ;
SLOTMAN, GJ ;
OPAL, SM ;
PRIBBLE, JP ;
BONE, RC ;
EMMANUEL, G ;
NG, D ;
BLOEDOW, DC ;
CATALANO, MA ;
FRIEDMAN, B ;
MURE, A ;
SHAPIRO, E .
CRITICAL CARE MEDICINE, 1994, 22 (01) :12-21
[9]   INFLUENCE OF AN ANTITUMOR NECROSIS FACTOR MONOCLONAL-ANTIBODY ON CYTOKINE LEVELS IN PATIENTS WITH SEPSIS [J].
FISHER, CJ ;
OPAL, SM ;
DHAINAUT, JF ;
STEPHENS, S ;
ZIMMERMAN, JL ;
NIGHTINGALE, P ;
HARRIS, SJ ;
SCHEIN, RMH ;
PANACEK, EA ;
VINCENT, JL ;
FOULKE, GE ;
WARREN, EL ;
GARRARD, C ;
PARK, G ;
BODMER, MW ;
COHEN, J ;
VANDERLINDEN, C ;
CROSS, AS ;
SADOFF, JC ;
GORECKI, J ;
DUBIN, HG ;
GARNER, C ;
KAYE, W ;
LANORE, JJ ;
MIRA, JP ;
ZIMMERMAN, J ;
DELLINGER, RP ;
TAYLOR, RW ;
DAHL, S ;
SHELLY, M ;
MORTIMER, A ;
EDWARDS, JD ;
KETT, DH ;
QUARTIN, A ;
PENA, MA ;
BAKKER, J ;
ALBERSON, TE ;
WALBY, W ;
RADCLIFFE, J ;
YOUNG, D ;
MCQUILLAM, P ;
BELLINGHAM, G ;
BURMAN, W ;
SADOFF, JS ;
YOUNG, L .
CRITICAL CARE MEDICINE, 1993, 21 (03) :318-327
[10]  
Foex BA, 1996, J ACCID EMERG MED, V13, P154