V. Zakusov Research Institute of Pharmacology, 8, Baltiiskaya str., 125315, Moscow, Russia.
Endocr Metab Immune Disord Drug Targets. 2022;22(8):834-841. doi: 10.2174/1871530322666220303162844.
Growing pieces of evidence demonstrate a close relationship between type 2 diabetes (T2D) and neurodegenerative disorders such as Alzheimer's disease. The similarity of physiological and pathological processes occurring in pancreatic β-cells and neurons over the course of these pathologies allows raising the question of the practicability of studying neuroprotective substances for their potential antidiabetic activity.
This review analyzes studies of antidiabetic and cytoprotective action on pancreatic β- cells of the neuroprotective compounds that can attenuate the oxidative stress and enhance the expression of neurotrophins: low-molecular-weight NGF mimetic compound GK-2, selective anxiolytic afobazole, antidepressants lithium chloride, and lithium carbonate on the rat streptozotocin model of T2D.
It was found that all the above-listed neuroprotective substances have a pronounced antidiabetic activity. The decrease in the β-cells number, the average area of the pancreatic islets, as well as the violation of their morphological structure caused by the streptozotocin was significantly weakened by the therapy with the investigated neuroprotective substances. The extent of these morphological changes clearly correlates with the antihyperglycemic effect of these compounds.
The presented data indicate that the neuroprotective substances attenuating the damaging effect of oxidative stress and neurotrophins deficit cannot only protect neurons but also exert their cytoprotective effect towards pancreatic β-cells. These data may provide a theoretical basis for the further study of neuroprotective drugs as potential therapeutic options for T2D prevention and treatment.
越来越多的证据表明 2 型糖尿病（T2D）与神经退行性疾病如阿尔茨海默病之间存在密切关系。在这些疾病过程中，胰腺β细胞和神经元中发生的生理和病理过程具有相似性，这使得人们提出了研究神经保护物质潜在的抗糖尿病活性的实用性问题。
本综述分析了具有抗糖尿病和对胰腺β细胞细胞保护作用的神经保护化合物的研究，这些化合物可以减轻氧化应激并增强神经营养因子的表达：低分子量 NGF 模拟物 GK-2、选择性抗焦虑药阿法唑仑、抗抑郁药氯化锂和碳酸锂在 T2D 的链脲佐菌素大鼠模型中的作用。
研究发现，所有上述列出的神经保护物质都具有明显的抗糖尿病活性。用研究中的神经保护物质治疗可显著减弱链脲佐菌素引起的β细胞数量减少、胰岛平均面积以及其形态结构的破坏。这些形态变化的程度与这些化合物的降血糖作用明显相关。
所提供的数据表明，减轻氧化应激和神经营养因子缺乏损伤作用的神经保护物质不仅可以保护神经元，还可以对胰腺β细胞发挥细胞保护作用。这些数据可能为进一步研究神经保护药物作为 T2D 预防和治疗的潜在治疗选择提供理论依据。
