丙烯酰胺母源性暴露对仔鼠海马齿状回DCX和GAP-43表达的影响

Expressions of DCX and GAP-43 in the hippocampal dentate gyrus of offspring rats after maternal exposure to acrylamide

目的检测丙烯酰胺(ACR)母源性暴露对仔鼠海马齿状回双皮质素(DCX)和生长相关蛋白-43(GAP-43)表达的影响,探讨ACR的神经发育毒性。方法孕鼠随机分为对照组(0 mg/kg)、ACR低(4.5 mg/kg)、中(9 mg/kg)和高(18 mg/kg)剂量组,每组8只,从妊娠第15天至分娩后第13天进行灌胃染毒。在分娩后第14天对仔鼠取材,通过免疫组织化学方法检测仔鼠海马齿状回DCX和GAP-43的表达。结果免疫组织化学方法结果显示,与对照组相比较,中、高剂量组孕鼠海马齿状回DCX和GAP-43的表达明显减少(P<0.05)。结论 ACR减少DCX和GAP-43的表达,可能干扰了神经元的生长发育。

Objective To investigate the neurodevelopmental toxicity of ACR by studying the expression of DCX and GAP- 43 in the hippocampal dentate gyms of rats after maternal exposure to acrylamide. Methods Pregnant rats were randomly divided into low-dose ACR （4.5 mg/kg ） , medium-dose （9 mg/kg ） , high dose groups （ 18 mg/kg） and the control group （0 mg/kg）, 8 in each group, and were exposed to toxicant from gestation- al day 15 to postnatal day 13. All rats and their pups were killed on postnatal day 14. ABC immunohistochemistry was used to detect the expression of GFAP in the hippocampus of mother rats and offspring. Results Compared with the control group, the expression of DCX and GAP-43 in hippocampus dentate gyms of the pregnant rats in middle and high dose groups was significantly decreased （P 〈 0.05 ）. Conclusion ACR may interfere with the growth and development of neurons by reducing the expression of DCX and GAP-43.