Abstract
Background
Glycine, pyruvate, resveratrol, and nitrite are well-known protective compounds among
others in ischemic tissue injury. Here, we compared their effects in acute lipopolysaccharide
(LPS)-induced shock in rats to assess whether inhibition of the proinflammatory cytokine
response is a prerequisite for their protective actions.
Materials and methods
Rats (six or eight per group) were anesthetized, received LPS as an intravenous bolus
(2.5 mg/kg), and were observed for 5 h. Glycine, sodium pyruvate, resveratrol, and
sodium nitrite were continuously infused starting 30 min before LPS administration.
Parameters included histopathologic changes, organ-specific cytokine levels, plasma
nitrite and nitrate concentrations, and time courses of biomonitoring parameters,
marker enzyme activities, and plasma cytokine concentrations.
Results
Glycine, pyruvate, resveratrol, and nitrite enhanced arterial blood pressure after
LPS-induced shock. Also, parameters reflecting tissue ischemia were significantly
improved and plasma markers of organ injury ameliorated by all substances. Of the
plasma cytokine concentrations increased by LPS, some were differently decreased or
even further increased by the substances. None of them reduced the elevated plasma
nitrite and nitrate concentration. Glycine diminished the increases in tissue cytokine
levels organ specifically, pyruvate decreased some cytokine concentrations in all
organs, and nitrite significantly affected only a few cytokine concentrations in some
organs, whereas the levels of many cytokines were raised by resveratrol. All substances
except resveratrol decreased granulocyte infiltrates in the liver.
Conclusions
The present results demonstrate that glycine, pyruvate, resveratrol, and nitrite protect
against LPS-induced shock and tissue injury (cell death) in rats and suggest that
inhibition of the proinflammatory cytokine response is not mandatory for their protective
actions.
Keywords
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Article info
Publication history
Published online: February 11, 2013
Accepted:
January 11,
2013
Received in revised form:
December 15,
2012
Received:
October 4,
2012
Identification
Copyright
© 2013 Elsevier Inc. Published by Elsevier Inc. All rights reserved.