Expression of α-smooth muscle actin and collagen I in lung fibroblasts of hyperoxia-exposed newborn rats

Objective To study the expression and the role of a-smooth muscle actin （a-SMA） and collagen I （Col I ） in lung fibroblasts of newborn rats with hyperoxia-induced lung injuries. Methods Thirty full-term newborn Wistar rats were randomly assigned to hyperoxia group （90% oxygen exposure, n = 15 ） and air group （ room air exposure, n -- 15 ） within 12 h after birth. Then lung ftbroblasts were isolated and primary cultured from rat lungs on postnatal 3 d ,7 d, and 14 d. The distribution of a-SMA protein were meas- ured by immunohistochemistry. The levels of Col I were detected by ELISA. Results There were no signif- icant differences in the levels of α-SMA and Col I expressions between the two groups at 3 d （ P 〉 0. 05 ）. While the expression of α-SMA （ 112. 60 ± 4. 61 vs 94. 69 ± 2. 38,200. 30 ± 3.97 vs 103.04 ± 1.91, P 〈 0. 01 ） and Col I protein [ （ 28. 66 ± 1.15 ） μg/L vs （ 24. 62 ± 3.15 ） μg/L, （ 30. 60 ± 0. 65 ） μg/L vs （27.46 ± 1.68 ） μg/L, P 〈 0. 05 ] in lung fibroblasts caused by hyperoxia were significantly higher than those in air-exposed group on postnatal 7 d and 14 d. There was positive correlation between α-SMA and Col I protein （ r = 0.72, P 〈 0.01 ）. Conclusion Hyperoxia promotes differentiation of lung fibroblasts into myofi- broblasts, and synthesis of type I collegen in neonatal rats, which leads to lung fibrosis finally. Key words: Hyperoxia;  Lung fibroblast;  et-Smooth muscle actin;  Myofibroblast;  Rat newborn