摘要
目的研究黄芪对大鼠放射性肺损伤(RILI)的保护作用及其机制。方法按照体重将SD雄性大鼠随机分成3组:空白对照组、模型组和实验组,每组12只。模型组和实验组大鼠的右肺部2 cm×3. 3 cm部位用直线加速器辐射,每周10 Gy,连续2周;空白对照组进行假辐射处理。辐照结束后第2天,实验组大鼠予以黄芪注射液0. 5 m L·kg~(-1)腹腔灌注,1次/天,连续9周,空白对照组与模型组予以相同体积0. 9%NaCl腹腔灌注。观察大鼠生存率,用免疫印迹法测定转化生长因子β1(TGF-β1)/Smads信号通路蛋白水平。结果空白对照组、模型组与实验组的大鼠肺指数分别为3. 77±0. 41,4. 86±1. 21和3. 90±0. 17;这3组的磷酸化Smad2/3蛋白表达的灰度值分别为0. 77±0. 13,1. 48±0. 26和0. 78±0. 09;这3组的TGF-β_1蛋白表达灰度值分别为1. 29±0. 18,1. 20±0. 27和0. 54±0. 13。上述指标,模型组与空白对照组比较或者实验组与模型组比较,差异均有统计学意义(均P <0. 05)。结论黄芪注射液可能主要通过抑制P-Smad2/3和TGF-β_1的蛋白量从而抑制肺纤维化的发展,并降低RILI的严重程度。
Objective To investigate the protective mechanism of Astragalus on radiation-induced lung injury( RILI) in rats. Methods SD male rats were randomly divided into three groups by weight: blank control group,model group and experimental group. Rats in model group and experimental group received 10 Gy/week by linear accelerator at 2. 0 cm × 3. 3 cm in the right lung region for 2 consecutive weeks. The blank control group received sham radiation treatment. The experimental group rats were given intraperitoneal perfusion with 0. 5 m L · kg~(-1) Astragalus injection once a day for 9 weeks since the end of irradiation. The blank control and model group rats were given intraperitoneal perfusion with normal saline. The survival rate and the right lung pathological section was observed in each group. The protein of the transforming growth factor-β_1( TGF-β_1)/Smads signal pathway was detected by Western blot.Results The lung index in blank control group,model group and experiment group were 3. 77 ± 0. 41,4. 86 ± 1. 21 and 3. 90 ± 0. 17,respectively. The p-Smad 2/3 expression( grey level) in the three groups were0. 77 ± 0. 13,1. 48 ± 0. 26 and 0. 78 ± 0. 09,respectively. The TGF-β_1 protein expression( grey level) in the three groups were 1. 29 ± 0. 18,1. 20 ± 0. 27 and 0. 54 ± 0. 13,respectively. Comparison between model group and blank control group or experimental group and model group,the difference of the factors were significantly( all P < 0. 05). Conclusion Astragalus injection may inhibit the development of pulmonary fibrosis and reduce the severity of RILI by inhibiting the protein content of p-Smad2/3 and TGF-β_1.
引文
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