JPEN. Journal of parenteral and enteral nutrition · 2007
Alanine-glutamine dipeptide (AGD) inhibits expression of inflammation-related genes in hemorrhagic shock.
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Yang Rongjie, Tan Xiaoyu, Thomas Ann M, Steppacher Robert, Qureshi Nilofer, Morrison David C, Van Way Charles W
Аннотация
BACKGROUND: Inflammatory factors play an important role in the production of cellular damage after shock and reperfusion. Glutamine has been used to modulate the inflammatory response. Alanine-glutamine dipeptide (AGD) is a glutamine source. The hypothesis of the present study is that AGD given during resuscitation will suppress postshock expression of messenger ribonucleic acid (mRNA) for tumor necrosis factor (TNF-alpha), interleukin-1 (IL-1beta) and inducible nitric oxide synthase (iNOS).
METHODS: Male Sprague-Dawley rats (n = 74, 350 g +/- 30 g) were randomly assigned to 5 groups. Under isoflurane anesthesia, the femoral artery and vein were cannulated. Hemorrhagic shock was induced by withdrawing blood through the arterial cannula until the mean arterial pressure (MAP) was 25-30 mm Hg and maintained at the level for 30 minutes with further withdrawals. Resuscitation was carried out by giving 21 mL/kg Ringer's lactate (LR) with or without the administration of AGD (936 mg/kg) and returning the shed blood. Controls were normal (anesthesia only), sham (surgical preparation), and shock (preparation and shock). Rats (n = 45, 9 per group) were killed 30 minutes after completion of resuscitation. Liver samples were collected, and total RNA was isolated for reverse transcription-polymerase chain reaction analysis of mRNA (TNF-alpha, IL-1beta, iNOS, and beta-actin).
RESULTS: MAP recovered more quickly in the AGD group than in the LR group. Increased expression of liver mRNA for TNF-alpha, IL-1beta, and iNOS was seen after hemorrhagic shock and resuscitation. AGD treatment significantly reduced mRNA expression for all 3.
CONCLUSIONS: AGD modified the expression of genes controlling cytokines and iNOS in the liver. This agent is a potential treatment for hemorrhagic shock.
METHODS: Male Sprague-Dawley rats (n = 74, 350 g +/- 30 g) were randomly assigned to 5 groups. Under isoflurane anesthesia, the femoral artery and vein were cannulated. Hemorrhagic shock was induced by withdrawing blood through the arterial cannula until the mean arterial pressure (MAP) was 25-30 mm Hg and maintained at the level for 30 minutes with further withdrawals. Resuscitation was carried out by giving 21 mL/kg Ringer's lactate (LR) with or without the administration of AGD (936 mg/kg) and returning the shed blood. Controls were normal (anesthesia only), sham (surgical preparation), and shock (preparation and shock). Rats (n = 45, 9 per group) were killed 30 minutes after completion of resuscitation. Liver samples were collected, and total RNA was isolated for reverse transcription-polymerase chain reaction analysis of mRNA (TNF-alpha, IL-1beta, iNOS, and beta-actin).
RESULTS: MAP recovered more quickly in the AGD group than in the LR group. Increased expression of liver mRNA for TNF-alpha, IL-1beta, and iNOS was seen after hemorrhagic shock and resuscitation. AGD treatment significantly reduced mRNA expression for all 3.
CONCLUSIONS: AGD modified the expression of genes controlling cytokines and iNOS in the liver. This agent is a potential treatment for hemorrhagic shock.