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目的通过观察镉暴露后胎盘组织形态结构和凋亡相关蛋白表达量的改变,探讨镉对胎盘组织中细胞增殖与凋亡的影响。方法将孕6天(E6)的20只孕鼠随机分成染镉组和对照组,染镉组一次性腹腔注射氯化镉,剂量为2mgCd/kg体重。两组的孕鼠分别于E14和E18断椎处死,每只孕鼠随机取出6个胎盘,制备石蜡切片。行HE染色观察染镉后胎盘的形态改变,免疫组织化学技术显示镉对Bcl-2和Bax表达的影响。结果染镉组胎盘海绵带滋养层细胞、巨细胞和空泡化细胞增多,且迷路带及海绵带滋养细胞呈退行性改变。染镉组胎盘组织细胞中的Bcl-2蛋白表达量比相应的对照组表达量明显降低(E14:t=7.067,P<0.01;E18:t=6.988,P<0.01);Bax蛋白表达量比相应的对照组表达量明显增多(E14:t=4.008,P<0.01;E18:t=4.732,P<0.01);Bcl-2/Bax比值与相应对照组之间的差异有统计学意义(E14:t=9.517,P<0.05;E18:t=23.380,P<0.01)。结论镉可以通过影响Bcl-2和Bax的表达,改变Bcl-2/Bax比值,使胎盘组织细胞的增殖和凋亡平衡紊乱,导致胎盘发育异常。
Objective To investigate the effect of cadmium on cell proliferation and apoptosis in placenta by observing the changes of placental morphology and apoptosis-related protein expression after exposure to cadmium. Methods Twenty pregnant pregnant rats of 6 days pregnant (E6) were randomly divided into cadmium group and control group. Cadmium chloride group was intraperitoneally injected with cadmium chloride at a dose of 2 mgCd / kg body weight. Two groups of pregnant rats were sacrificed on the E14 and E18 vertebra respectively, and 6 placenta were randomly removed from each pregnant rat to prepare paraffin sections. The morphological changes of placenta were observed with HE staining, and the effect of cadmium on the expression of Bcl-2 and Bax was detected by immunohistochemistry. Results The placental sponge with trophoblast cells in the cadmium group had increased giant cells and vacuolated cells, and the trophoblastic cells in the lost zone and the sponge belts showed degenerative changes. The expression of Bcl-2 protein in placental tissue of cadmium-exposed group was significantly lower than that of corresponding control group (E14: t = 7.067, P <0.01; E18: t = 6.988, P <0.01) (E14: t = 4.008, P <0.01; E18: t = 4.732, P <0.01). The difference between Bcl-2 / Bax ratio and corresponding control group was statistically significant (E14: : t = 9.517, P <0.05; E18: t = 23.380, P <0.01). Conclusion Cadmium can affect the expression of Bcl-2 and Bax and change the ratio of Bcl-2 / Bax, resulting in the imbalance of proliferation and apoptosis of placental cells, leading to abnormal placental development.