Department of Nutrition and Food Hygiene, West China School of Public Health, Sichuan University, Chengdu 610041, Sichuan Province, China ; Department of Nutrition, Institute of Health & Environmental Medicine, Academy of Military Medical Sciences, Tianjin 300050, China.
Department of Hepatobiliary Surgery, Children's Hospital, Chongqing Medical University, Chongqing 400014, China.
Neural Regen Res. 2013 Oct 15;8(29):2754-62. doi: 10.3969/j.issn.1673-5374.2013.29.007.
Zinc supplementation can help maintain learning and memory function in rodents. In this study, we hypothesized that zinc supplementation could antagonize the neurotoxicity induced by aluminum in rats. Animals were fed a diet containing different doses of zinc (50, 100, 200 mg/kg) for 9 weeks, and orally administered aluminum chloride (300 mg/kg daily) from the third week for 7 consecutive weeks. Open-field behavioral test results showed that the number of rearings in the group given the 100 mg/kg zinc supplement was significantly increased compared with the group given the 50 mg/kg zinc supplement. Malondialdehyde content in the cerebrum was significantly decreased, while dopamine and 5-hydroxytryptamine levels were increased in the groups given the diet supplemented with 100 and 200 mg/kg zinc, compared with the group given the diet supplemented with 50 mg/kg zinc. The acetylcholinesterase activity in the cerebrum was significantly decreased in the group given the 100 mg/kg zinc supplement. Hematoxylin-eosin staining revealed evident pathological damage in the hippocampus of rats in the group given the diet supplemented with 50 mg/kg zinc, but the damage was attenuated in the groups given the diet supplemented with 100 and 200 mg/kg zinc. Our findings suggest that zinc is a potential neuroprotective agent against aluminum-induced neurotoxicity in rats, and the optimal dosages are 100 and 200 mg/kg.
锌补充剂可帮助维持啮齿动物的学习和记忆功能。在这项研究中,我们假设锌补充剂可以拮抗铝在大鼠体内引起的神经毒性。动物喂食含有不同剂量锌(50、100、200mg/kg)的饮食 9 周,并从第 3 周开始连续 7 天每天口服给予氯化铝(300mg/kg)。旷场行为测试结果表明,给予 100mg/kg 锌补充剂的组的后肢次数明显多于给予 50mg/kg 锌补充剂的组。大脑中海马体的丙二醛含量明显降低,而给予 100 和 200mg/kg 锌补充饮食的组的多巴胺和 5-羟色胺水平升高,与给予 50mg/kg 锌补充饮食的组相比。给予 100mg/kg 锌补充的组大脑中的乙酰胆碱酯酶活性明显降低。苏木精-伊红染色显示,给予 50mg/kg 锌补充饮食的组大鼠海马体有明显的病理损伤,而给予 100 和 200mg/kg 锌补充饮食的组损伤减轻。我们的研究结果表明,锌是一种潜在的神经保护剂,可对抗铝诱导的大鼠神经毒性,最佳剂量为 100 和 200mg/kg。