PURPOSE: Pulmonary fibrosis (PF) is characterized by fibroblasts proliferation, excessive deposition of collagen and extracellular matrix remodeling due to inflammatory processes, such as reactive oxygen species’ generation and apoptosis. Erythropoietin (EPO) is a multiple functional cytokine with anti-oxidative, anti-inflammatory and anti-apoptotic properties. Aim of this study was to examine the effects of EPO on bleomycin (BLM)-induced lung fibrosis in rats.
METHODS: Twenty-one Wistar rats (300g) were devided into three groups: Group 1 (n=7): intratracheal injection of BLM hydrochloride (7.5 mg/kg), Group 2 (n=7): intratracheal BLM injection (7.5 mg/kg) followed by EPO intraperitoneal injection (2000 u/kg),Group 3 (n=7): saline (0.5 ml/kg) intratracheal injection (control group). All rats were sacrificed after 14 days. Histological evaluation was performed on paraffin sections stained with hematoxyline-eosin. Lung injury was estimated quantitatively in 15 randomly selected fields/slide by Image Pro Plus software version 4.1. Mean score was defined as the percentage of lung injury of all fields. Statistical analysis was performed; a p value less than 0.05 was considered statistically significant.
RESULTS: Group 1 showed dense interstitial infiltration by inflammatory cells mainly lymphocytes, neutrophils and fibroplasts and foci of fibrotic lesions especially in peribronchial regions. Group 2 manifested suppression of the BLM-induced inflammatory cellular infiltration and fibrotic lesions. Group 3 displayed normal lung structure with no pathological changes. Lesions in Group 2 were markedly less severe compared to those of Group 1. (40.64±11.31% vs 69.72±2.63%, p<0.05).
CONCLUSION: Treatment with EPO significantly ameliorated the extent and severity of the BLM-induced toxicity in lung tissue. Additional studies are required to clarify the underlying mechanisms of the protective action of EPO on lung fibrosis.
CLINICAL IMPLICATIONS: Our findings suggest that EPO may serve as a novel target for potential therapeutic treatment of lung fibrosis.
DISCLOSURE: Drosos Tsavlis, None.