论文部分内容阅读
目的探讨孕鼠叶酸缺乏对新生大鼠肺泡Ⅱ型细胞超微结构及转化生长因子-β1(TGF-β1)/Smads信号通路的影响。方法成熟雌性Sprague-Dawley大鼠36只,随机分为实验组和对照组(各18只),分别喂以缺乏叶酸和添加叶酸的纯合饲料。2周后与雄性大鼠交配。取新生大鼠肺组织标本,采用透射电子显微镜观察新生大鼠肺泡Ⅱ型细胞超微结构,采用实时荧光定量PCR法检测新生大鼠肺组织中TGF-β1、Smad2和Smad3的mRNA表达水平。结果 1.叶酸缺乏组新生大鼠肺泡Ⅱ型细胞胞质内含较多絮状物,板层小体和细胞器难见。对照组肺泡Ⅱ型细胞胞质内的板层小体发达,且板层小体染色深,结构清晰、致密,胞质内可见发达的线粒体等细胞器。2.叶酸缺乏组新生大鼠肺组织TGF-β1及Smad3 mRNA表达低于对照组,差异均有统计学意义(Pa<0.05),叶酸缺乏组新生大鼠肺组织Smad2 mRNA表达与对照组比较差异无统计学意义(P>0.05)。结论叶酸缺乏可影响子代肺泡Ⅱ型细胞结构改变,并可能通过影响TGF-β1/Smads信号通路延缓或阻碍肺组织发育。
Objective To investigate the effect of folic acid deficiency in pregnant rats on the ultrastructure of alveolar type Ⅱ cells and the signal transduction of transforming growth factor-β1 (TGF-β1) / Smads in neonatal rats. Methods Thirty-six adult female Sprague-Dawley rats were randomly divided into experimental group and control group (18 rats each), and fed with pure fodder without folic acid and folic acid respectively. Male rats mated 2 weeks later. Lung tissue samples were taken from newborn rats. The ultrastructure of alveolar type Ⅱ cells in neonatal rats was observed by transmission electron microscopy. The mRNA expression of TGF-β1, Smad2 and Smad3 in lungs of neonatal rats was detected by real-time fluorescence quantitative PCR. Folic acid deficiency group neonatal alveolar type Ⅱ cells contain more cytoplasm within the cytoplasm, lamina propria and organelles is difficult to see. The cytoplasm of the alveolar type Ⅱ cells in the control group developed well in the cytoplasm, and the lamellar bodies were deeply stained, the structures were clear and dense, and the organelles such as mitochondria were found in the cytoplasm. Compared with control group, the expression of TGF-β1 and Smad3 mRNA in lung tissue of neonatal rats with folic acid deficiency group was significantly lower than that of control group (P <0.05). The expression of Smad2 mRNA in lung tissue of neonatal rats with folic acid deficiency group was significantly lower than that of control group No statistical significance (P> 0.05). Conclusion Folic acid deficiency can affect the alveolar type Ⅱ cell structure changes and may delay or hinder the development of lung tissue by affecting TGF-β1 / Smads signaling pathway.