Evaluation of the Effects of Nicotinamide on the Bleomycin-induced Pulmonary Fibrosis in Rat

Fibrosis is the abnormal production of collagen fibers following tissue damage. This accounts for the formation of scar tissue. Lung fibrosis is one of the typical ways in which the lung reacts to damaging stimuli. In this study we tried to investigate the involving phenomena during the process of bleomycin-induced fibrosis in murine lung. We have evaluated this process at three levels, namely, at (1) cellular level (cells with contraction activity of pulmonary tissue), (2) intercellular signaling agents (e.g., IL-8, TNF-, TGF-$), tissue index factors (collagen, hydroxyproline) and some inorganic elements which may hypothetically be engaged as efficient enzymatic cofactors (e.g., copper), (3) pathophysiological or exaggerated physiological processes (inflammation and fibrosis). The pharmacological agent which have been selected for evaluating in this study is Nicotinamide, which their selection rationale will be discussed in detail separately in the discussion section. Bleomycin-induced pulmonary fibrosis is a widely used animal model for lung injury and fibrosis. After single dose instillation of intratracheal bleomycin, the fibrotic responses were studied by biochemical measurement of collagen deposition and analysis of pathological lung changes in different treatment groups. The results of this study showed that administrated agents in different doses, had satisfactorily healing effects on fibrosis process, ranging from good to moderate, through significant decreasing in lung collagen content (p<0.05).