Nicotinamide abrogates acute lung injury caused by ischaemia/reperfusion

Poly (ADP-ribose) synthase or polymerase (PARS and PARP, respectively) is a cytotoxic enzyme which causes cellular damage. Nicotinamide, a compound of vitamin B complex, has been reported to exert an inhibitory effect on PARS or PARP. The present study tests the effects of nicotinamide on acute lung...

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Published in:The European respiratory journal Vol. 30; no. 2; p. 199
Main Authors: Su, C-F, Liu, D D, Kao, S J, Chen, H I
Format: Journal Article
Language:English
Published: England 01.08.2007
Subjects:
Adenosine Triphosphate - metabolism
Analysis of Variance
Animals
Disease Models, Animal
Free Radicals
Interleukin-1 - metabolism
Ischemia - pathology
Lung - blood supply
Lung - metabolism
Lung - pathology
Lung Injury
Male
Methylguanidine - metabolism
Niacinamide - pharmacology
Nitric Oxide - metabolism
Nitric Oxide Synthase - metabolism
Poly(ADP-ribose) Polymerases - metabolism
Rats
Rats, Sprague-Dawley
Reperfusion Injury - drug therapy
Reperfusion Injury - pathology
Tumor Necrosis Factor-alpha - metabolism
ISSN:0903-1936
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Summary:Poly (ADP-ribose) synthase or polymerase (PARS and PARP, respectively) is a cytotoxic enzyme which causes cellular damage. Nicotinamide, a compound of vitamin B complex, has been reported to exert an inhibitory effect on PARS or PARP. The present study tests the effects of nicotinamide on acute lung injury and associated alterations following ischaemia/reperfusion (I/R) of the isolated perfused rat's lung. I/R increased the lung weight (LW) to body weight ratio, LW gain, protein and dye tracer leakage, pulmonary arterial pressure and capillary permeability. The insult also increased nitrate/nitrite, methyl guanidine, tumour necrosis factor-alpha and interleukin-1beta in lung perfusate, while it decreased adenosine triphosphate content with an increase in PARP activity in lung tissue. Most of the I/R-induced changes were abrogated by post-treatment (30 min after I/R) with nicotinamide (100 mg.kg(-1) body weight). However, the increase in pulmonary arterial pressure was enhanced by nicotinamide post-treatment. Following I/R, the inducible nitric oxide synthase (iNOS) mRNA expression was enhanced. Nicotinamide reduced the iNOS expression. The results suggest that nicotinamide exerted a protective effect on the acute lung injury caused by ischaemia/reperfusion. The mechanisms may be mediated through the inhibition on the poly (adenosine diphosphate-ribose) polymerase activity, inducible nitric oxide synthase expression and the subsequent suppression of nitric oxide, free radicals and pro-inflammatory cytokines with restoration of adenosine triphosphate.
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ISSN:0903-1936
DOI:10.1183/09031936.00025107