Song Lingzhen, Wang Jiutao, Zhang Wei, Yan Runchuan, Hu Xinde, Chen Shulin, Zhao Shanting
College of Veterinary Medicine, Northwest A&F University, Yangling, 712100, Shaanxi, People's Republic of China.
Neurochem Res. 2014 Nov;39(11):2170-9. doi: 10.1007/s11064-014-1418-8. Epub 2014 Aug 22.
The primary objective of this investigation was to assess the neuroprotective efficacy of lithium in an acrylamide (ACR)-induced neuropathy model in mice. In this study, Kunming male mice were administered ACR (25 mg/kg bw, i.p. once a day) with or without lithium (25 mg/kg bw, i.p. once a day) for 2 weeks. All ACR-administered mice exhibited severe symptoms of neuropathy. We found that treatment with lithium effectively alleviated behavioral deficits in animals elicited by acrylamide. Interestingly, the reduction of hippocampal neurogenesis resulting from ACR injection was promoted by administration of lithium. Further, lithium treatment significantly offset ACR-induced depletion in p-GSK-3β (Ser9) levels in hippocampus. Collectively our findings suggest the propensity of lithium to attenuate ACR-induced neuropathy. Further studies are necessary to understand the precise molecular mechanism by which the lithium attenuates neuropathy. Nevertheless, our data clearly demonstrate the beneficial effects of lithium on ACR-induced neuropathy in mice and suggest its possible therapeutic application as an adjuvant in the management of other forms of neuropathy in humans.
本研究的主要目的是评估锂在小鼠丙烯酰胺（ACR）诱导的神经病变模型中的神经保护作用。在本研究中，对昆明雄性小鼠给予ACR（25mg/kg体重，腹腔注射，每天一次），同时或不同时给予锂（25mg/kg体重，腹腔注射，每天一次），持续2周。所有给予ACR的小鼠均表现出严重的神经病变症状。我们发现，锂治疗可有效减轻丙烯酰胺引起的动物行为缺陷。有趣的是，锂的给药促进了ACR注射导致的海马神经发生减少。此外，锂治疗显著抵消了ACR诱导的海马中p-GSK-3β（Ser9）水平的降低。我们的研究结果共同表明，锂具有减轻ACR诱导的神经病变的倾向。有必要进行进一步的研究以了解锂减轻神经病变的精确分子机制。然而，我们的数据清楚地证明了锂对小鼠ACR诱导的神经病变的有益作用，并表明其作为辅助药物在人类其他形式神经病变管理中的可能治疗应用。
