| 摘要: |
| 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30 d。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。 |
| 关键词: 苯并芘 维生素E 神经毒性 氧化性应激 |
| DOI：10.3724/SP.J.1008.2015.01295 |
| 投稿时间：2015-06-05修订日期：2015-08-21 |
| 基金项目:国家自然科学基金(81372957). |
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| Effect of vitamin E against the neurotoxicity induced by benzo[a]pryene in adult rats |
| LI Wei1,LIANG Xiao1,LUO Long1,ZHANG Xiao-ying1,YANG Kai1,WU Meng-yun2,TU Bai-jie1* |
(1. School of Public Health and Management, Center for Research of Medicine & Social Development, Innovation Center for Social Risk Governance in Health, Chongqing Medical University, Chongqing 400016, China;
2. Laboratory of Reproductive Biology, School of Public Health, Chongqing Medical University, Chongqing 400016, China
*Corresponding author.) |
| Abstract: |
| Objective To explore the effect of vitamin E (VE) against the neurotoxicity of benzo[a]pryene (B[a]P) in male SD rats. Methods A total of 60 male SD rats were randomly assigned to one of the following six groups (n=10/group): the blank control group, vehicle control group, B[a]P group(5 mg/kg), low dose of VE (10 mg/kg) + B[a]P (5 mg/kg) group, medium dose of VE (50 mg/kg) + B[a]P (5 mg/kg) group and high dose of VE (100 mg/kg) + B[a]P (5 mg/kg) group. The rats were gavaged with the corresponding dose of B[a]P once a day for 30 days. Morris water maze was used to evaluate the learning and memory performance of rats. Morphological changes in hippocampus were observed. The activities of superoxide dismutase(SOD), glutathione peroxidase(GSH-Px) and γ-glutamylcysteine synthetase(γ-GCS), the contents of glutathione(GSH), oxidized glutathione (GSSG) and malonaldehyde (MDA) in the hippocampus tissue were all examined. Results The results of the behavior tests showed that rats treated with B[a]P exhibited a significantly increased escape latency and a significantly decreased cross-platform times and the residence time on the platform compared with the blank control group and vehicle group (P<0.01). VE treatment could obviously improve the changes of the above index (P<0.01). Besides, the morphological changes in hippocampus suggested that VE could protect against the injury induced by B[a]P. The activities of SOD, GSH-Px and γ-GCS and the contents of GSH, GSSG in rat hippocampus of B[a]P group were significantly decreased, while the content of MDA was significantly increased compared with the blank control group and vehicle control group (P<0.01). Moreover, the above indices were obviously improved with the increase of VE dosage in VE groups. Conclusion VE can play an protective role in B[a]P-induced neurotoxicity. |
| Key words: benzo[a]pyrene vitamin E neurotoxicity oxidative stress |
