Nicotinamide abrogates acute lung injury caused by ischemia-reperfusion

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

^* To whom correspondence should be addressed. E-mail: chenhi{at}mail.tcu.edu.tw.

	Abstract

Poly (ADP-ribose) synthase (PARS) or polymerase (PARP) is cytotoxic enzyme causing cellular damage. Nicotinamide, a compound of vitamin B complex, has been reported to exert inhibitory effect on PAPS or PARP. The present experiment tests the effects of nicotinamide on acute lung injury (ALI) and associated alterations following ischemia-reperfusion (I/R) of the isolated perfused rat's lung.

I/R increased 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-1 in lung perfusate, while decreased adenosine triphosphate (ATP) content with an increase in PARP activity in lung tissue.

Most of the I/R-induced chagnes 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 protective effect on the ALI caused by I/R. The mechanisms may be mediated through the inhibition on the PARP activity, iNOS expression and the subsequent suppression of nitric oxide, free radicals, and proinflammatory cytokines with restoration of ATP.

This article has been cited by other articles:

				J. Sun, D. Yang, S. Li, Z. Xu, X. Wang, and C. Bai Effects of curcumin or dexamethasone on lung ischaemia-reperfusion injury in rats Eur. Respir. J., February 1, 2009; 33(2): 398 - 404. [Abstract] [Full Text] [PDF]

				S. C. Cheng, D. O. Young, Y. Huang, J. A. Delmez, and D. W. Coyne A Randomized, Double-Blind, Placebo-Controlled Trial of Niacinamide for Reduction of Phosphorus in Hemodialysis Patients Clin. J. Am. Soc. Nephrol., July 1, 2008; 3(4): 1131 - 1138. [Abstract] [Full Text] [PDF]