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目的探讨孕期全氟辛烷磺酸(PFOS)暴露诱导的胎鼠肺损伤中糖皮质激素影响。方法通过低、中、高(5、10、20 mg/kg)剂量PFOS对孕期SD大鼠染毒7 d,于受孕第19 d取胎鼠全肺采用实时荧光聚合酶链式反应、western blot及酶联免疫吸附试验检测胎鼠肺脏中糖皮质激素含量及相关调控基因mRNA、蛋白表达。结果与对照组比较,PFOS组胎鼠肺脏中糖皮质激素含量有升高趋势;高剂量PFOS组11β-羟基类固醇脱氢酶1(11βHSD1)mRNA表达(99.07±15.06)高于对照组(P<0.05),11βHSD2 mRNA表达(1.140±0.303 2)明显低于对照组(P<0.01),11βHSD2蛋白水平低于对照组(P<0.05);与对照组比较,高剂量PFOS组己糖-6-磷酸脱氢酶(H6PDH)mRNA(21.37±3.013)升高(P<0.05);肺表面活性物质相关蛋白C(SP-C)表达无明显变化。结论孕期PFOS暴露诱导的胎鼠肺损伤中,糖皮质激素未发生明显变化,推测肺损伤不是肺表面张力破坏引起的。
Objective To investigate the effects of glucocorticoid on fetal lung injury induced by exposure to PFOS during pregnancy. Methods The pregnant SD rats were exposed to low, medium and high dose (5,10,20 mg / kg) of PFOS for 7 days. Real-time fluorescence polymerase chain reaction (FQ-PCR) ELISA and enzyme-linked immunosorbent assay were used to detect the content of glucocorticoid in fetal lungs and the mRNA and protein expression of related regulatory genes. Results Compared with the control group, the content of glucocorticoid in the lungs of PFOS group increased significantly. The mRNA expression of 11β-hydroxysteroid dehydrogenase 1 (11βHSD1) in high dose PFOS group (99.07 ± 15.06) was higher than that in the control group (P < 0.05), and the expression of 11βHSD2 mRNA (1.140 ± 0.303 2) was significantly lower than that of the control group (P <0.01) and the level of 11βHSD2 protein was lower than that of the control group (P <0.05) (P <0.05). There was no significant difference in the expression of surfactant protein C (SP-C) between H6PDH mRNA and H7PDH mRNA (21.37 ± 3.013). Conclusions There is no significant change of glucocorticoid in fetal lung injury induced by PFOS exposure during pregnancy. It is speculated that lung injury is not caused by the destruction of pulmonary surface tension.