Title of article :
Dietary glycine inhibits activation of nuclear factor kappa B and prevents liver injury in hemorrhagic shock in the rat
Author/Authors :
J. L. Mauriz، نويسنده , , B. Matilla، نويسنده , , J. M. Culebras، نويسنده , , P. Gonz?lez، نويسنده , , J. Gonz?lez-Gallego، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2001
Abstract :
We investigated the effects of a glycine-containing diet (5%) on liver injury caused by hemorrhagic shock and resuscitation in rats. Anesthetized rats were bled to a mean arterial blood pressure of 35–40 mm Hg for 1 h and then resuscitated with 60% of shed blood and lactated Ringer’s solution. Feeding the rats glycine significantly reduced mortality, the elevation of plasma transaminase levels and hepatic necrosis. The increase in plasma TNFα and nitric oxide (NO) was also blunted by glycine feeding. Hemorrhagic shock resulted in oxidative stress (significant elevations in TBARS and in the oxidized/reduced glutathione ratio) and was accompanied by a reduced activity of the antioxidant enzymes Mn- and Cu,Zn-superoxide dismutase, glutathione peroxidase and catalase, overexpression of inducible NO synthase (iNOS), and activation of nuclear factor kappa B (NF-κB). Glycine ameliorated oxidative stress and the impairment in antioxidant enzyme activities, inhibited NF-κB activation, and prevented expression of iNOS. Dietary glycine blocks activation of different mediators involved in the pathophysiology of liver injury after shock.
Keywords :
antioxidant enzymes , Glycine , Hemorrhagic shock , oxidative stress , free radicals , nitric oxide , glutathione , nuclear factor ?B
Journal title :
Free Radical Biology and Medicine
Journal title :
Free Radical Biology and Medicine