Comparison of Bleomycin-Induced Pulmonary Apoptosis Between Nmri Mice and C57bl/6 Mice



Safaeian L¹ ; Jafarian A¹ ; Rabbani M¹ ; Sadeghi HM² ; Afsharmoghaddam N³ ; Sarahroodi S⁴ Show Affiliations
Source: Research in Pharmaceutical Sciences Published:2013

Abstract

Apoptosis has a critical role in the pathogenesis of bleomycin induced-pulmonary fibrosis. The severity of fibrosis varies among different strains of mice. Recent studies have indicated that expression of apoptotic regulatory genes may be specific in different cell types in various strains. In this study, bleomycin-induced pulmonary apoptosis in NMRI (Naval Medical Research Institute, USA) albino mice were compared with C57BL/6 black mice. Pulmonary fibrosis induced by single intratracheal administration of bleomycin (3 U/kg). Control mice were instilled with the same volume of saline. After 2 weeks, fibrotic responses were studied by biochemical measurement of collagen deposition and histological examination of pathological lung changes. Apoptosis was detected and quantitated by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Bleomycin significantly (P<0.05) increased lung collagen content and also induced fibrotic histological changes in both strains. Apoptosis was detected in the bronchiolar and alveolar epithelial cells after bleomycin instillation. TUNEL-positive alveolar epithelial cells in bleomycintreated lungs of C57BL/6 and NMRI mice (19.5% ± 2.7 and 17% ± 2.0, respectively) were significantly (P<0.05) higher than that of saline-treated lungs (1.5% ± 0.5) with no significant difference between two strains of mice (P>0.05). Despite some murine strain variation in the expression of apoptotic regulatory genes in bleomycin-induced pulmonary fibrosis, the results of the present study revealed no significant differences in alveolar epithelial apoptosis between NMRI and C57BL/6 black mice. However, these results confirm the role of apoptosis in the pathogenesis of pulmonary fibrosis and suitability of both strains as experimental models of lung fibrosis.