Carnosine is an endogenously synthesized dipeptide composed by -alanine and L-histidine. It acts as a free radical scavenger and possesses antioxidant properties. Carnosine reduces pro-inflammatory and pro-fibrotic cytokines such as TGF-, IL-1 and TNF- in different experimental settings. In the present study, we investigated the efficacy of carnosine on the animal model of bleomycin-induced lung injury. Mice were subjected to intra-tracheal administration of bleomycin and were assigned to receive carnosine daily by an oral bolus of 150 mg/Kg. One week after fibrosis induction, BAL cell counts and TGF- levels, lung histology and immunohistochemical analysis for myeloperoxidase, TGF-, inducible nitric oxide synthase (iNOS), nitrotyrosine, and poly-ADP-ribose polymerase (PARP) were performed. Finally, apoptosis was quantified by TUNEL assay. Following bleomycin administration, carnosine treated mice exhibited a reduced degree of lung damage and inflammation when compared to WT mice as shown by the reduction of:(i)loss of body weight, (ii)mortality rate, (iii)lung infiltration by neutrophils (myeloperoxidase activity, BAL total and differential cell counts), (iv)lung edema, (v)histological evidence of lung injury and collagen deposition, (vi)lung myeloperoxidase, TGF-, iNOS, nitrotyrosine and PARP immunostaining, (vii)BAL TGF- levels and (viii)apoptosis. Our results indicate that orally administered carnosine is able to prevent bleomycin induced lung injury likely through its direct antioxidant properties. Carnosine is already available for human use. It might prove useful as an add-on therapy for the treatment of fibrotic disorders of the lung where oxidative stress plays a role such as idiopathic pulmonary fibrosis, a disease that still represents a major challenge to medical treatment.