The effect of N-acetyl cysteine on serum glutathione, TNF-α and tissue malondialdehyde levels in the treatment of sepsis

被引:11
作者
Gul, Mehmet [2 ]
Ayan, Murat [1 ]
Seydanoglu, Abdusselam [1 ]
Cander, Basar [2 ]
Girisgin, Sadik [2 ]
Erayman, Ibrahim [3 ]
Erdem, Sami [4 ]
机构
[1] Gaziosmanpasa Univ, Tip Fak, Acil Tip Anabilim Dali, Tokat, Turkey
[2] Selcuk Univ, Meram Fac Med, Dept Emergency Med, Konya, Turkey
[3] Selcuk Univ, Meram Fac Med, Dept Infect Dis, Konya, Turkey
[4] Selcuk Univ, Meram Fac Med, Dept Biochem, Konya, Turkey
来源
ULUSAL TRAVMA VE ACIL CERRAHI DERGISI-TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY | 2011年 / 17卷 / 04期
关键词
Glutathione; N-acetyl cysteine; sepsis; tumor necrosis factor-alpha; malondialdehyde; CECAL LIGATION; ACETYLCYSTEINE; ENDOTOXEMIA; MODEL; LUNG; RATS; PUNCTURE; INJURY; DAMAGE; BRAIN;
D O I
10.5505/tjtes.2011.66743
中图分类号
R4 [临床医学];
学科分类号
100218 [急诊医学];
摘要
BACKGROUND The aim of this study was to investigate the effects of N-acetyl cysteine (NAC) on the levels of reactive oxygen species in sepsis. METHODS In this study, 30 Sprague-Dawley female rats weighing 180-200 g were used. Rats were randomized into three groups, each containing 10 rats, as follows: Group I: Sham, Group II: Sepsis and Group III: Sepsis+NAC. Group I underwent only laparotomy. In Groups II and III, sepsis was induced by cecal ligation and perforation (CLP) technique. NAC (20 mg/kg/day) was administered orally to Group III at 0, 8 and 16 hours. At the 24th hour, tissue and blood samples were taken for erythrocyte glutathione (GSH) and serum tumor necrosis factor (TNF)-alpha levels, histopathological determination, and lung, liver and kidney tissue malondialdehyde (MDA) analyses. RESULTS Group III was significantly different from the other groups with respect to erythrocyte glutathione, serum TNF-alpha and kidney MDA levels (p<0.05). There was no significant difference between the groups regarding liver MDA levels and histopathological parameters for lung, liver and kidney (p>0.05). CONCLUSION NAC treatment had beneficial effects on erythrocyte GSH, serum TNF-alpha, lung function, and kidney MDA levels in sepsis-induced rats. However, this beneficial effect was not confirmed as histopathological improvement. Further research is needed to prove the effect of NAC in sepsis treatment.
引用
收藏
页码:293 / 297
页数:5
相关论文
共 18 条
[1]
The sepsis syndrome - Definition and general approach to management [J].
Bone, RC .
CLINICS IN CHEST MEDICINE, 1996, 17 (02) :175-&
[2]
N-acetylcysteine exerts protective effects and prevents lung redox imbalance and peroxynitrite generation in endotoxemic rats [J].
Carbonell, Luis F. ;
Diaz, Julian ;
Hernandez, Isabel ;
Cuevas, Santiago ;
Valero, Fernando ;
Quesada, Tomas ;
Fenoy, Francisco ;
Salom, Miguel G. .
MEDICINAL CHEMISTRY, 2007, 3 (01) :29-34
[3]
Effects of N-Acetylcysteine/Deferoxamine, Taurine and RC-3095 on Respiratory Chain Complexes and Creatine Kinase Activities in Rat Brain After Sepsis [J].
Cassol, Omar J., Jr. ;
Rezin, Gislaine T. ;
Petronilho, Fabricia C. ;
Scaini, Giselli ;
Goncalves, Cinara L. ;
Ferreira, Gabriela K. ;
Roesler, Rafael ;
Schwartsmann, Gilberto ;
Dal-Pizzol, Felipe ;
Streck, Emilio L. .
NEUROCHEMICAL RESEARCH, 2010, 35 (04) :515-521
[4]
Cetinkaya A, 2006, MED SCI MONITOR, V12, pBR274
[5]
Cotgreave I A, 1997, Adv Pharmacol, V38, P205
[6]
Is there a place for N-acetylcysteine in the treatment of septic shock? [J].
Del Sorbo, L ;
Zhang, HB .
CRITICAL CARE, 2004, 8 (02) :93-95
[7]
Post-treatment with N-acetylcysteine ameliorates endotoxin shock-induced organ damage in conscious rats [J].
Hsu, Bang-Gee ;
Lee, Ru-Ping ;
Yang, Fwu-Lin ;
Harn, Horng-Jyh ;
Chen, Hsing I. .
LIFE SCIENCES, 2006, 79 (21) :2010-2016
[8]
KANSU E, 2005, YOGUN BAKIM ENFEKSIY, P381
[9]
Exogenous surfactant and partial liquid ventilation - Physiologic and pathologic effects [J].
Mrozek, JD ;
Smith, KM ;
Bing, DR ;
Meyers, PA ;
Simonton, SC ;
Connett, JE ;
Mammel, MC .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1997, 156 (04) :1058-1065
[10]
N-acetylcysteine suppresses TNF-induced NF-κB activation through inhibition of IκB kinases [J].
Oka, S ;
Kamata, H ;
Kamata, K ;
Yagisawa, H ;
Hirata, H .
FEBS LETTERS, 2000, 472 (2-3) :196-202