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目的探讨维生素E(VE)对苯并[a]芘(benzo[a]pryene,B[a]P)所致雄性SD大鼠神经毒性的拮抗作用。方法将60只SD雄性大鼠随机分为空白、溶剂对照组、B[a]P组及VE低、中、高联合B[a]P处理组,每组10只。连续灌胃30d。通过Morris水迷宫测试大鼠学习记忆能力;观察海马形态学改变以及海马组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、谷氨酰半胱氨酸合成酶(γ-GCS)活性及谷胱甘肽(GSH)、氧化型谷胱甘肽(GSSG)、丙二醛(MDA)含量变化。结果行为学结果显示B[a]P组大鼠较对照组平均逃避潜伏期升高,跨台次数和在原平台象限停留时间降低,差异有统计学意义(P<0.01);而VE可改善各指标变化(P<0.01)。此外,海马神经形态学变化提示VE可拮抗B[a]P的损害作用;与对照组比较,B[a]P组大鼠海马组织SOD、GSH-Px、γ-GCS活性以及GSH、GSSG含量下降,MDA含量上升,差异均有统计学意义(P<0.01),且随着VE剂量增加,各指标均逐渐改善。结论 VE对B[a]P导致的神经毒性具有拮抗作用。
Objective To investigate the antagonism of vitamin E (VE) on neurotoxicity in male SD rats induced by benzo [a] pyrene (B [a] P). Methods Sixty SD male rats were randomly divided into blank control group, B [a] P group and low, middle and high VE combined with B [a] P group, 10 rats in each group. Continuous gavage 30d. Morris water maze was used to test the learning and memory abilities of rats. The morphological changes of hippocampus and the changes of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutamylcysteine (Γ-GCS) activity and glutathione (GSH), oxidized glutathione (GSSG), malondialdehyde (MDA) content. Results The results of behavioral study showed that the mean escape latency of rats in B [a] P group was significantly higher than that of the control group (P <0.01), while the number of transits and residence time in the original platform quadrant decreased significantly Change (P <0.01). In addition, neuronal morphological changes in hippocampus suggested that VE could antagonize the damage of B [a] P. Compared with the control group, the activity of SOD, GSH-Px, γ-GCS and the contents of GSH and GSSG in hippocampus of B [ (P <0.01). With the increase of dose of VE, all the indexes improved gradually. Conclusion VE antagonizes the neurotoxicity induced by B [a] P.