[The expression of α-smooth muscle actin during the lung injury induced by hyperoxia].

Yue-qiang Fu, Cheng-jun Liu, Jing Li, Lan Hu, Zhong-yi Lu, Feng Xu
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Abstract

OBJECTIVE To explore the expression of α-smooth muscle actin (α-SMA) during the lung injury induced by hyperoxia in infantile rats. METHODS Sixty-four male Sprague-Dawley (SD) rats about 3 weeks were randomly assigned into normal control group which exposured to room air [fraction of inspired oxygen (FiO(2)) was 0.21] and hyperoxia exposure group (95%O(2)) according to random digits table. Eight rats in each group were randomly sacrificed at day 1, 7, 14 and 21.Pulmonary tissue remodeling was observed by hematoxylin-eosin (HE) staining. Immunohistochemistry method was performed to evaluate the expression of α-SMA in pulmonary tissue, further Western blotting was also made to determine the expression of α-SMA. RESULTS The early histopathologic changes after HE were inflammation and edema in pulmonary tissue, while the later changes were interstitial hyperplasia and fibroblast proliferation. The expression of α-SMA was very slight in bronchial epithelium, alveolar epithelium and alveolar interstitium in normal control group, but increased with the time of hyperoxia exposure prolonged and peaked at 21st day. Western blotting detected that the expression of α-SMA after hyperoxia exposure for 1 day and 7 days in hyperoxia exposure group presented no difference compared with normal control group (1.02±0.12 vs. 1.00±0.13, 1.05±0.14 vs. 0.99±0.12, both P>0.05), but the expression of α-SMA after hyperoxia exposure for 14 days and 21 days was increased compared with normal control group (1.27±0.21 vs. 1.05±0.15, 2.26±0.28 vs. 1.05±0.14, P<0.05 and P<0.01). CONCLUSIONS Pulmonary fibrosis remodeling was caused by hyperoxia exposure. The expression of α-SMA in pulmonary tissue in hyperoxia exposure groups obviously increased, and could play an important role in pulmonary fibrosis remodeling.
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[α-平滑肌肌动蛋白在高氧肺损伤中的表达]。
目的探讨α-平滑肌肌动蛋白(α-SMA)在幼年大鼠高氧肺损伤中的表达。方法将64只3周龄雄性SD大鼠按随机数字表法随机分为室内空气暴露正常对照组[吸入氧分数(FiO(2) = 0.21]和高氧暴露组(95%O(2))。各组随机于第1、7、14、21天处死8只大鼠。苏木精-伊红(HE)染色观察肺组织重构。免疫组化法检测肺组织α-SMA的表达,免疫印迹法检测肺组织α-SMA的表达。结果HE术后早期病理表现为肺组织炎症和水肿,晚期病理表现为间质增生和成纤维细胞增生。正常对照组大鼠支气管上皮、肺泡上皮和肺泡间质α-SMA表达极低,但随高氧暴露时间延长而升高,在第21天达到峰值。Western blot检测高氧暴露1 d、7 d后α-SMA表达量与正常对照组比较差异无统计学意义(1.02±0.12 vs 1.00±0.13,1.05±0.14 vs 0.99±0.12,P均>0.05),高氧暴露14 d、21 d后α-SMA表达量与正常对照组比较差异有统计学意义(1.27±0.21 vs 1.05±0.15,2.26±0.28 vs 1.05±0.14,P<0.05、P<0.01)。结论肺纤维化重构与高氧暴露有关。高氧暴露组肺组织α-SMA表达明显升高,可能在肺纤维化重构中发挥重要作用。
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