转化生长因子β_3对早产大鼠肺表面活性物质蛋白质基因表达的影响及机理  

The effects and mechanism of TGF β 3 on the expressions of pulmonary surfactant proteins in premature rat lung

作　　者：王晓川[1] 金勤立[1] 徐锦[1] 沈惟堂[1] 

机构地区：[1]上海医科大学儿科医院

出　　处：《中华儿科杂志》1997年第4期180-182,共3页Chinese Journal of Pediatrics

基　　金：国家自然科学基金;国家教委博士点基金

摘　　要：为研究转化生长因子β３（ＴＧＦ－β３）对发育期肺表面活性物质蛋白质（ＳＰｓ）基因表达的影响。利用孕１９天早产大鼠肺组织块及肺Ⅱ型细胞培养，检测ＳＰｓ（ＳＰ－Ａ、ＳＰ－Ｂ和ＳＰ－Ｃ）基因表达。结果：单纯使用ＴＧＦ－β３对ＳＰ－Ａ、ＳＰ－Ｂ、ＳＰ－Ｃ基因表达无明显影响，但ＴＧＦ－β３可明显抑制１００ｎｍｏｌ／ｍｌ地塞米松增加ＳＰ－Ｂ、ＳＰ－Ｃ基因表达的效应，随ＴＧＦ－β３浓度增加抑制显著。ＴＧＦ－β３并非直接作用于肺Ⅱ型上皮细胞，而是以成纤维细胞为介导产生抑制效应。ＴＧＦ－β３对地塞米松增加ＳＰ－Ａ基因表达无影响。提示：ＴＧＦ－β３对肺发育期ＳＰｓ基因表达有抑制作用，糖皮质激素预防新生儿呼吸窘迫综合征效果不理想可能与ＴＧＦ－β３作用有关。To determine the effects of transforming growth factor β 3 (TGF β 3 ) on the expressions of surfactant proteins (SP), the authors employed premature rats 19 days of gestational age to detect the SP A,SP B and SP C mRNA levels in cultured lung explants and type Ⅱcells. The results of the study showed that TGF β 3 alone did not affect the expressions of SPs either in explants or in type Ⅱcells, however, TGF β 3 did significantly inhibit the increase of SP B, SP C mRNA levels by dexamethasone (100 nM) in a dose dependent manner. Furthermore, TGF β 3 had no direct inhibitory effect on the increase of SP B, SP C mRNA induced by dexamethasone in type Ⅱ cells, but by fibroblasts indirectly. The authors conclude that TGF β 3 plays an important inhibitory role in the development of pulmonary surfactant proteins and that the present study may provide a possible explanation for the unideal effects of glucocorticid in prevention of neonatal respiratory distress syndrome.

关 键 词：转化生长因子Β SPS 呼吸窘迫综合征 新生儿 

分 类 号：R563[医药卫生—呼吸系统] R362[医药卫生—内科学]