孕鼠弓形虫感染对胎盘激素水平的影响

Effects of Toxoplasma gondii infection on placenta hormones in pregnant BALB/c mice

目的通过检测弓形虫感染孕鼠胎盘分泌的胰岛素生长因子-Ⅱ(IGF-Ⅱ)含量和11β-羟基类固醇脱氢酶-2(11β-HSD2)的表达,分析弓形虫感染对孕鼠胎盘激素水平和胎鼠发育的影响。方法腹腔接种弓形虫速殖子0.2ml/只(含50个速殖子)感染孕8d小鼠,分别于感染后12、14、16和18d处死,取胎盘组织,用酶联免疫吸附试验检测IGF-Ⅱ含量,用免疫组织化学法检测11β-HSD2的表达。未感染孕鼠做健康对照。结果健康对照组孕鼠胎盘组织IGF-Ⅱ含量随妊娠天数的增加逐渐升高,弓形虫感染组IGF-Ⅱ含量先降低后升高。IGF-Ⅱ含量不同妊娠天数组内比较差异有统计学意义(P<0.05),相同妊娠天数组间比较差异有统计学意义(P<0.05)。11β-HSD2含量,不同妊娠天数健康对照鼠差异有统计学意义(P<0.05),不同妊娠天数弓形虫感染鼠含量差异无统计学意义(P>0.05);妊娠14d、16d、18d组间差异有统计学意义(P<0.05)。结论弓形虫感染鼠孕中期,胎盘IGF-Ⅱ含量及11β-HSD2表达降低,可能影响胎盘血管形成及糖原合成与转运及进入胎儿体内糖皮质激素的含量,从而导致胎儿发育异常。

Objective To analyze the effects of Toxoplasma gondii infection on the hormones by detecting the concentration of insulin-like growth factors（IGF-Ⅱ） and the levels of 11β-hydroxysteroid dehydrogenase-2（11β-HSD2）expression in the placentae of pregnant BALB/c mice.Methods Pregnant mice were infected with T.Gondii on the 8th day of pregnancy,and pregnant mice were sacrificed on the 12th,14th,and 16th day of pregnancy.The placentae of pregnant mice were collected,and the percentage of IGF-Ⅱ was determined with ELISA.The level of 11β-HSD2 expression was determined immunohistochemically.Results An IGF-Ⅱ assay showed that the concentration increased as pregnancy continued in the normal control group but first decreased and then increased in the infected group.Differences in IGF-Ⅱ levels at different days of gestation were statistically significant（P0.05） in both groups,and differences in those levels at the same days of gestation were statistically significant（P0.05）.The expression of 11β-HSD2 increased as pregnancy continued in the normal control group.Differences in 11β-HSD2 levels at different days of gestation were statistically significant（P0.05）in the normal control group,and levels did not differ（P0.05） in the infected group.Differences in 11β-HSD2 levels at the same days of gestation were statistically significant（P0.05）.Conclusion In pregnant mice infected with T.gondii,the secretion of the 11β-HSD2 and IGF-Ⅱ decreased.This may be due to the concentration of GC in mice fetuses,blood vessels,and glycogen synthesis and transport in the placenta.These changes may delay the growth of fetal mice in the womb.