Mohd Sairazi Nur Shafika, K N S Sirajudeen, Asari Mohd Asnizam, Mummedy Swamy, Muzaimi Mustapha, Sulaiman Siti Amrah
Department of Chemical Pathology, School of Medical Sciences, Universiti Sains Malaysia, Health Campus, 16150 Kubang Kerian, Kota Bharu, Kelantan, Malaysia.
Department of Anatomy, School of Medical Sciences, Universiti Sains Malaysia, Health Campus, 16150 Kubang Kerian, Kota Bharu, Kelantan, Malaysia.
BMC Complement Altern Med. 2017 Jan 9;17(1):31. doi: 10.1186/s12906-016-1534-x.
Administration of KA on rodents has resulted in seizures, behavioral changes, oxidative stress, and neuronal degeneration on selective population of neurons in the brain. The present study was undertaken to investigate the extent of neuroprotective effect conferred by Malaysian Tualang Honey (TH), an antioxidant agent, in the cerebral cortex of rats against KA-induced oxidative stress and neurodegeneration in an animal model of KA-induced excitotoxicity.
Male Sprague-Dawley rats were randomly divided into five groups: Control, KA-treated group, TH + KA-treated group, aspirin (ASP; anti-inflammatory agent) + KA-treated group and topiramate (TPM; antiepileptic agent) + KA-treated group. The animals were pretreated orally with drinking water, TH (1.0g/kg BW), ASP (7.5mg/kg BW) or TPM (40mg/kg BW), respectively, five times at 12 h intervals. KA (15mg/kg BW) was injected subcutaneously 30 min after last treatment to all groups except the control group (normal saline). Behavioral change was observed using an open field test (OFT) to assess the locomotor activity of the animals. Animals were sacrificed after 2 h, 24 h and 48 h of KA administration.
KA significantly inflicted more neuronal degeneration in the piriform cortex and heightened the predilection to seizures as compared with the control animals. Pretreatment with TH reduced the KA-induced neuronal degeneration in the piriform cortex but failed to prevent the occurrence of KA-induced seizures. In the OFT, KA-induced animals showed an increased in locomotor activity and hyperactivity and these were attenuated by TH pretreatment. Furthermore, TH pretreatment significantly attenuated an increase of thiobarbituric acid reactive substances level and a decrease of total antioxidant status level enhanced by KA in the cerebral cortex.
These results suggest that pretreatment with TH has a therapeutic potential against KA-induced oxidative stress and neurodegeneration through its antioxidant effect.
给啮齿动物注射海人酸（KA）会导致癫痫发作、行为改变、氧化应激以及大脑中特定神经元群体的神经退行性变。本研究旨在探讨马来西亚蜂酿蜜（TH）这种抗氧化剂在大鼠大脑皮层中对KA诱导的兴奋性毒性动物模型的氧化应激和神经退行性变所赋予的神经保护作用程度。
将雄性Sprague-Dawley大鼠随机分为五组：对照组、KA处理组、TH + KA处理组、阿司匹林（ASP；抗炎药）+ KA处理组和托吡酯（TPM；抗癫痫药）+ KA处理组。分别给动物口服饮用水、TH（1.0g/kg体重）、ASP（7.5mg/kg体重）或TPM（40mg/kg体重）进行预处理，每隔12小时一次，共五次。除对照组（生理盐水）外，在最后一次处理后30分钟给所有组皮下注射KA（15mg/kg体重）。使用旷场试验（OFT）观察行为变化以评估动物的运动活性。在注射KA后2小时、24小时和48小时处死动物。
与对照动物相比，KA显著导致梨状皮质中更多的神经退行性变，并增加了癫痫发作的倾向。TH预处理减少了KA诱导的梨状皮质中的神经退行性变，但未能预防KA诱导的癫痫发作的发生。在旷场试验中，KA诱导的动物表现出运动活性增加和多动，而TH预处理减弱了这些表现。此外，TH预处理显著减弱了KA在大脑皮层中增强的硫代巴比妥酸反应性物质水平的升高和总抗氧化状态水平的降低。
这些结果表明，TH预处理通过其抗氧化作用对KA诱导 的氧化应激和神经退行性变具有治疗潜力。
