Synergetic Treatment of Ascorbic Acid and Nicotine Ameliorates Aluminium Induced Neurotoxicity in the Prefrontal Cortex of Wistar Rat

T. Abayomi
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Abstract

Background: Though the neuroprotective roles of ascorbic acid are well established, the therapeutic role of nicotine in various neurological disorders is attracting increasing attention. This study evaluated the putative ameliorative role of the synergetic treatment of nicotine and ascorbic acid against neurodegenerative consequences associated with free radical species and amyloid plaques generation in adult male Wistar rats Methods: A total of 35 Wistar rats were distributed into five groups labeled A-E. Group A served as the control group; animals in group B were treated with 100mg/kg body weight of aluminium chloride (AlCl3) for 21 days. Group C animals were treated with 100mg/kg body weight of aluminium chloride for 21 days and post-treated with 14mg/kg body weight of nicotine for 21 days. Group D was treated with 100mg/kg body weight of aluminium chloride for 21 days and post-treated with 100mg/kg bodyweight of ascorbic acid for 21 days. Group E animals were treated with 100mg/kg body weight of aluminium chloride for 21 days and post-treated with 100mg/kg bodyweight of ascorbic acid and 14mg/kg body weight of nicotine. On completion of treatments, the prefrontal cortex was excised and processed for biochemical and histochemical examinations. Results: Oxidative stress was evident from the diminished level of catalase and glutathione per oxidase and elevated lipid peroxidation levels in animals administered with aluminium in addition to the presence of amyloid plaques in these animals. However, synergetic administration of ascorbic acid and nicotine attenuated these oxidative and histochemical perturbations induced by aluminium. Conclusion: Synergetic treatment with ascorbic acid and nicotine provided better ameliorative potential against aluminium-induced neurotoxicity compared to either ascorbic acid or nicotine treatments alone
抗坏血酸和尼古丁协同治疗可改善铝诱导的Wistar大鼠前额皮质神经毒性
背景:虽然抗坏血酸的神经保护作用已被证实,但尼古丁在各种神经系统疾病中的治疗作用正引起越来越多的关注。本研究评估了尼古丁和抗坏血酸协同治疗对成年雄性Wistar大鼠与自由基种类和淀粉样斑块产生相关的神经退行性后果的可能改善作用。方法:35只Wistar大鼠分为5组,标记为A- e。A组为对照组;B组用100mg/kg体重的氯化铝(AlCl3)处理21 d。C组小鼠给予100mg/kg体重氯化铝21 d,后给予14mg/kg体重尼古丁21 d。D组给予100mg/kg体重的氯化铝处理21 D,后给予100mg/kg体重的抗坏血酸处理21 D。E组小鼠给予100mg/kg体重的氯化铝21 d,后给予100mg/kg体重的抗坏血酸和14mg/kg体重的尼古丁。治疗结束后,切除前额叶皮层,进行生化和组织化学检查。结果:氧化应激从过氧化氢酶和谷胱甘肽每氧化酶水平的降低和脂质过氧化水平的升高中可以明显看出,除了这些动物中淀粉样斑块的存在。然而,抗坏血酸和尼古丁的协同施用可以减轻铝引起的氧化和组织化学扰动。结论:与单用抗坏血酸或尼古丁治疗相比,抗坏血酸和尼古丁协同治疗对铝诱导的神经毒性有更好的改善潜力
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