Abstract

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

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