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Nicotinamide abrogates acute lung injury caused by ischaemia/reperfusion

¹ Dept of Neurosurgery and ² Neuro-Medical Scientific Center, Tzu Chi Hospital and University, ³ Dept of Dentistry, Tzu Chi Hospital and ⁶ Institute of Integrative Physiology and Clinical Sciences, Tzu Chi University, Hualien, and ⁴ Division of Chest Medicine, Internal Medicine, Shin-Kong Wu-Ho-Su Memorial Hospital, School of Respiratory Therapy, Taipei Medical University, and ⁵ College of Medicine, Fu-Jen University, Taipei, Taiwan.

CORRESPONDENCE: H. I. Chen, Institute of Integrative Physiology and Clinical Sciences, Tzu Chi University, No. 701 Sec. 3, Jhongyang Rd., Hualien 97004, Taiwan. Fax: 886 38573053. E-mail: chenhi{at}mail.tcu.edu.tw

Keywords: Free radical, inducible nitric oxide synthase, nitric oxide, poly (ADP-ribose) polymerase, pro-inflammatory cytokines

Received: March 2, 2007
Accepted April 30, 2007

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- and interleukin-1ß 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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