Abdulmajeed Wahab Imam, Sulieman Habeeb Bolakale, Zubayr Maymunah Oloruntosin, Imam Aminu, Amin Abdulbasit, Biliaminu Sikiru Abayomi, Oyewole Lukuman Aboyeji, Owoyele Bamidele Victor
Department of Physiology Faculty of Basic Medical Sciences, University of Ilorin, Ilorin, Nigeria.
Department of Anatomy, Faculty of Basic Medical Sciences, University of Ilorin, Ilorin, Nigeria.
Metab Brain Dis. 2016 Feb;31(1):37-44. doi: 10.1007/s11011-015-9733-6. Epub 2015 Oct 5.
This research sought to investigate the possible neuroprotective effects of honey against lead (Pb)-induced neurotoxicity. Twenty four male Wistar rats were divided into four groups: Control group that received 1 ml/kg distilled orally for 28 days; while groups II-IV received 0.2% lead in drinking water and 1 ml/kg of distilled water, 1 ml/kg of honey, 1.5 ml/kg of honey respectively for 28 days. Anxiety and exploratory activities were determined in the open field test. Memory function was determined using Morris water maze after which the animals were sacrificed. The brains were then excised, homogenized and Lipid peroxidation (MDA), Superoxide dismutase (SOD), Catalase, Glutathione (GSH) and Glutathione -S- Transferase (GST) activities were determined in the brains. Results showed that lead exposure causes decrease in locomotor and exploratory activities; increase anxiety, memory impairment, lipid peroxidation and decrease antioxidant activities. However, co-administration of honey with lead inhibited neurotoxicity as indicated by the improvement in memory function as evidenced by decreased latency period and increased in time spent in target quadrant in honey-fed rats compared to the lead-exposed animals. Furthermore, honey increased locomotion, exploration and decreased anxiety in lead-exposed rats as indicated by the frequency of rearing, freezing duration and the number of line crossed by animals. Also administration of honey improves antioxidant activities as shown by increased brain SOD, GST and GSH activities compared to the lead-treated groups but no significant effect on MDA level. It can be concluded that honey has neuroprotective effects against lead-induced cognitive deficit probably by enhancing antioxidant activities.
本研究旨在探讨蜂蜜对铅（Pb）诱导的神经毒性可能具有的神经保护作用。将24只雄性Wistar大鼠分为四组：对照组口服1 ml/kg蒸馏水，持续28天；而第二至四组在饮用水中加入0.2%的铅，并分别给予1 ml/kg蒸馏水、1 ml/kg蜂蜜、1.5 ml/kg蜂蜜，持续28天。通过旷场试验测定焦虑和探索活动。使用莫里斯水迷宫测定记忆功能，之后处死动物。然后取出大脑，进行匀浆，并测定大脑中的脂质过氧化（MDA）、超氧化物歧化酶（SOD）、过氧化氢酶、谷胱甘肽（GSH）和谷胱甘肽-S-转移酶（GST）活性。结果表明，铅暴露会导致运动和探索活动减少；焦虑增加、记忆受损、脂质过氧化增加以及抗氧化活性降低。然而，与铅暴露动物相比，蜂蜜与铅共同给药可抑制神经毒性，这表现为记忆功能改善，如蜂蜜喂养组大鼠的潜伏期缩短以及在目标象限停留时间增加所证明。此外，如通过动物的竖毛频率、静止持续时间和穿越线条数量所示，蜂蜜可增加铅暴露大鼠的运动、探索并减轻焦虑。而且，与铅处理组相比，给予蜂蜜可提高抗氧化活性，如大脑SOD、GST和GSH活性增加，但对MDA水平无显著影响。可以得出结论，蜂蜜可能通过增强抗氧化活性对铅诱导的认知缺陷具有神经保护作用。
