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目的:探讨母源性丙烯酰胺(acrylamide,ACR)暴露对子代鼠大脑皮质神经元MAP-2与氧化应激的影响。方法:SD孕鼠随机分为4组,自怀孕第6 d至怀孕第19 d起对照组和实验组分别灌胃给药给予双蒸水和每日8,16和24 mg/kg ACR溶液。HE和尼氏染色观察子代鼠皮质神经元形态学改变,免疫组织化学和Western Blot检测子代鼠皮质神经元MAP-2的表达,应用试剂盒检测大脑皮质组织中氧化应激指标丙二醛(MDA)、总超氧化物歧化酶(T-SOD)、还原谷胱甘肽(GSH)。结果:(1)MAP-2表达:与对照组相比,实验组中、高剂量组MAP-2表达下降,差异有统计学意义(P<0.05),而低剂量组则差异不显著(P>0.05)。(2)氧化应激指标变化:与对照组相比,实验组中、高剂量组子代鼠大脑皮质组织中MDA含量显著升高,而T-SOD活力和GSH含量显著下降,差异具有统计学意义(P<0.05)。结论:丙烯酰胺致子代鼠神经元损伤的机制可能与其诱导氧化应激损伤有关。
Objective: To investigate the effects of maternal acrylamide (ACR) exposure on MAP-2 and oxidative stress in cortical neurons of offspring mice. Methods: Pregnant SD rats were randomly divided into 4 groups. From the 6th day of pregnancy to the 19th day of pregnancy, the control group and the experimental group were orally administered with distilled water and 8, 16 and 24 mg / kg ACR solution daily. Morphological changes of cortical neurons were observed by HE staining and Nissl’s staining. The expression of MAP-2 in cortical neurons of offspring rats was detected by immunohistochemistry and Western Blot. The oxidative stress indicators such as malondialdehyde (MDA), total superoxide dismutase (T-SOD), reduced glutathione (GSH). Results: (1) The expression of MAP-2: Compared with the control group, the expression of MAP-2 in the experimental group and the high-dose group decreased significantly (P <0.05), while there was no significant difference in the low-dose group > 0.05). (2) The changes of oxidative stress index: Compared with the control group, in the experimental group, the content of MDA in the cerebral cortex tissue of the high dose group was significantly increased, while the T-SOD activity and GSH content were significantly decreased, the difference was statistically Significance (P <0.05). Conclusion: The mechanism of acrylamide induced neuronal damage may be related to its induction of oxidative stress injury.