| Abstract: | Bleomycin (BLM)-induced lung fibrosis has been shown to be accompanied by the activation of poly(ADP-ribose) polymerase and depletion of nicotinamide adenine dinucleotide (NAD) in the lung. Niacin, a precursor of NAD, was used in the present study to investigate its possible ameliorating effect on BLM-induced pulmonary fibrosis in hamsters. Niacin (500 mg/kg IP) or saline (IP) was injected daily for 16 or 23 days. On day 3, hamsters were treated with BLM (7.5 U/5 mL/kg) or an equivalent volume of saline intratracheally. BLM alone significantly increased lung hydroxyproline levels, bron-choalveolar lavage fluid protein concentration, and various inflammatory cell counts in the lavage in both experiments. In addition, BLM alone elevated prolyl hydroxylase and poly(adenosine-5′-diphosphate [ADP]-ribose) polymerase activities in the 3-week study. Niacin treatment significantly decreased BLM-elevated lung hydroxyproline, prolyl hydroxylase, and poly(ADP-ribose) polymerase activities. Histopa-thology revealed that niacin treatment attenuated BLM-induced thickened alveolar septa, foci of fibrotic consolidation, and accumulations of inflammatory cells in the parenchyma and air spaces. The ability of niacin to attenuate BLM-induced lung fibrosis in hamsters suggests that it may have potential as an antifibrotic agent in humans. |
