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目的探讨发育关键期双酚A(BPA)暴露对海马齿状回(DG)区突触形成和树突棘的影响及其机制。方法出生7 d的SD大鼠,腹腔注射BPA 50,250和500μg·kg-1·d-1,连续7 d。Golgi-Cox染色分析海马DG区树突棘密度和树突棘头形态大小,Western blotting检测β联蛋白,Wnt7a及Wnt5a蛋白表达。结果 BPA 50,250和500μg·kg-1组海马DG区树突棘密度依次为9.67±0.17,8.97±0.13,(8.71±0.15)/10μm,相对于正常对照组的(10.21±0.17)/10μm,BPA 50,250和500μg·kg-1·d-1组树突棘密度显著下降(P<0.05)。正常对照组树突棘头为(0.67±0.03)μm2,BPA 50,250和500μg·kg-1组树突棘头依次为0.53±0.03,0.51±0.03和(0.50±0.03)μm2,显著低于正常对照组(P<0.05)。BPA 50,250和500μg·kg-1·d-1组磷酸化的β联蛋白占总体β联蛋白的百分比分别提高了18.28%,32.22%和57.01%,而Wnt7a表达显著降低(P<0.05),Wnt5a表达显著提高(P<0.05)。结论在BPA所引起的突触形成和树突棘的损伤中,Wnt信号通路可能起关键作用。
Objective To investigate the effects of BPA exposure on the synapse formation and dendritic spines in the dentate gyrus (DG) area of hippocampus and its mechanism. Methods Sprague Dawley (SD) rats 7 days after birth were injected intraperitoneally with BPA 50, 250 and 500 μg · kg-1 · d-1 for 7 days. The dendritic spines density and dendritic spine head morphology of hippocampal DG were analyzed by Golgi-Cox staining. The protein expressions of β-catenin, Wnt7a and Wnt5a were detected by Western blotting. Results The density of dendritic spines in the hippocampus DG of 50, 250 and 500μg · kg-1 groups were 9.67 ± 0.17, 8.97 ± 0.13, (8.71 ± 0.15) / 10μm respectively, compared with that of the normal control group (10.21 ± 0.17) / 10μm, BPA Dendritic spine density in 50, 250 and 500μg · kg-1 · d-1 groups decreased significantly (P <0.05). The dendritic spines in the normal control group were (0.67 ± 0.03) μm2, and the dendritic spines in the BPA 50, 250 and 500 μg · kg-1 groups were 0.53 ± 0.03, 0.51 ± 0.03 and 0.50 ± 0.03 μm2, respectively, which were significantly lower than those in the normal control Group (P <0.05). The percentages of phosphorylated β-catenin in the BPA 50, 250 and 500 μg · kg -1 · d -1 groups were increased by 18.28%, 32.22% and 57.01%, respectively, while the expression of Wnt7a was significantly decreased (P <0.05) The expression was significantly increased (P <0.05). Conclusion The Wnt signaling pathway may play a key role in the synapse formation and dendritic spines damage induced by BPA.