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suffering from different pulmonary fibrosis variations, IPF, sarcoidosis wherein it is noted
that NAC improved BAL fluid glutathione of the considered patients for the researches
(Meyer et al., 1994; Behr et al., 1997). In studies which utilised the rat and mice models of
bleomycin-induced fibrosis revealed that NAC acts as a inhibitor of different mechanism of
profibrosis such as the amounts of collagen, hydroxyproline, cytokines, mucus secretory cells
and the mucin subtype 5ac (Behr et al., 1997; Cortijo et al., 2001; Serrano-Mollar et al., 2003;
Mata et al., 2003). NAC is also known to inhibit the transition of epithelial–mesenchyma in
the alveolar epithelial cells of rat models (Felton et al., 2009). wherein it is also known to
reduce the contraction of TGF-β-induced gel, production of VEGF and the expression of α-
SMA in the fibroblasts of human lungs (Sugiura et al., 2009). Furthermore, NAC tends to
reduce the concentrations of cytokines in IPF patients generated by alveolar macrophages
(Radomska-Leśniewska et al., 2010)(Patel et al., 2012). Several recent studies involving
animal models revealed that NAC reduced the score of fibrosis, protects lung injury,
decreases the content of reactive oxygen species in the macrophages of alveolus (Wang et al.,
2013; Zhang et al., 2013, 2014).
Figure 2: Timeline of N-acetylcysteine
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