M. Ito, A. Suwabe, T. Suzuki, M. Tominaga, K. Takahashi
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引用次数: 3
摘要
我们研究了人工表面活性剂是否能改变大鼠气管内给药博来霉素(BLM 3.75 mg/kg)后的肺纤维化。博莱霉素给药24小时后,用表面活性剂- ta (S-TA, 1 mg/ml, 6 ml × 2次)洗涤肺部2次,并用10 mg/ml S-TA 0.5 ml代替。14天后处死,检测肺组织胶原蛋白含量及病理变化。blm处理的大鼠肺湿重和肺胶原含量均增加,体重下降(由于肺损伤和纤维化),但气管内给药S-TA显著抑制了这些变化。体外研究表明,S-TA抑制肺成纤维细胞增殖呈剂量依赖性(0.01 ~ 0.5 mg/ml)。这种抑制作用也见于天然大鼠肺表面活性剂及其蛋白和脂质组分。然而,S-TA并没有改变培养中的大鼠II型肺炎细胞的数量,并且可能保护II型细胞免于去分化。S-TA抑制blm诱导的肺纤维化,可能是通过直接抑制肺成纤维细胞增殖。
[The effects of surfactant-TA on bleomycin-induced lung injury and lung fibroblast proliferation].
We investigated whether artificial surfactant modified pulmonary fibrosis following the intratracheal administration of bleomycin (BLM 3.75 mg/kg) in rats. Twenty-four hours after the administration of bleomycin, the lungs were washed twice with surfactant-TA (S-TA, 1 mg/ml, 6 ml x 2 times), and replaced with 0.5 ml of 10 mg/ml S-TA. Fourteen days later the animals were sacrificed and the lungs were assayed for collagen content and pathologic changes. BLM-treated rats showed both increases in wet lung weights and lung collagen content, and a loss in body weights (due to lung injury and fibrosis), but these changes were significantly inhibited by the intratracheal administration of S-TA. In vitro studies demonstrated that S-TA inhibited lung fibroblast proliferation in a dose dependent manner (0.01-0.5 mg/ml). This inhibition was also seen in native rat lung surfactant and its protein and lipid components. However, S-TA, did not change the number of rat type II pneumocutes in culture, and likely protected type II cells from dedifferentiation. S-TA inhibited BLM-induced pulmonary fibrosis, probably by directly inhibiting lung fibroblast proliferation.