论文部分内容阅读
目的制备高体积分数氧(高氧)诱导新生大鼠慢性肺疾病(CLD)模型,探讨持续吸入高氧对新生大鼠肺组织及成纤维细胞Bax及Bcl-2蛋白表达的影响。方法足月新生大鼠出生12h内分别持续吸入氧体积分数为900 mL·L-1的高氧(高氧组)和空气(空气组),于3d、7d和14d随机处死动物后,肺组织取材同时进行肺成纤维细胞的原代培养,应用免疫组织化学半定量法检测其Bax及Bcl-2蛋白水平变化。结果在肺组织中,高氧组Bcl-2蛋白的表达水平在7d、14d有所升高(P<0.001),3 d时表达无变化(P>0.05);而高氧组Bax蛋白的表达水平及Bax/Bcl-2比值在3d、7d和14d均明显高于空气组,且具有时间敏感性(Pa<0.01)。在肺成纤维细胞,高氧组3d、7d Bcl-2蛋白表达水平无变化(P>0.05),14 d时有所增高(P<0.001),但不如Bax蛋白增加明显;高氧组3d、7d和14d肺成纤维细胞Bax蛋白的表达水平及Bax/Bcl-2比值均明显高于空气组(Pa<0.01)。结论高氧可促进新生大鼠肺组织及成纤维细胞Bax蛋白的表达,从而通过上调Bax/Bcl-2比值促进凋亡发生,参与CLD的发生发展过程。
OBJECTIVE: To establish a model of chronic lung disease (CLD) induced by high volume fraction oxygen (hyperoxia) in neonatal rats and investigate the effect of sustained inhalation of hyperoxia on Bax and Bcl-2 protein expression in lung and fibroblasts of neonatal rats. Methods The neonatal rats were exposed to hyperoxia (high oxygen group) and air (air group) with an oxygen concentration of 900 mL · L-1 for 12 hours after birth, respectively. After sacrificed at 3d, 7d and 14d, The primary cultured lung fibroblasts were also harvested at the same time. The protein levels of Bax and Bcl-2 were detected by semi-quantitative immunohistochemistry. Results In lung tissue, the expression of Bcl-2 protein in hyperoxia group was increased at 7d and 14d (P <0.001), but not at 3 days (P> 0.05). The expression of Bax protein in hyperoxia group The levels and Bax / Bcl-2 ratios were significantly higher than those of air group at 3d, 7d and 14d (P <0.01). In lung fibroblasts, the expression of Bcl-2 protein in the hyperoxia group did not change at 3d and 7d (P> 0.05), but increased at 14d (P <0.001) The expression of Bax and Bax / Bcl-2 in lung fibroblasts at 7d and 14d were significantly higher than those in air group (Pa <0.01). Conclusion Hyperoxia can promote the expression of Bax protein in lung tissue and fibroblasts of newborn rats, and promote the development of CLD by up-regulating Bax / Bcl-2 ratio.