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首页> 外文期刊>Journal of Neurochemistry: Offical Journal of the International Society for Neurochemistry >Neuroprotective effects of vildagliptin in rat rotenone Parkinson's disease model: role of RAGE-NF kappa B and Nrf2 antioxidant signaling pathways
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Neuroprotective effects of vildagliptin in rat rotenone Parkinson's disease model: role of RAGE-NF kappa B and Nrf2 antioxidant signaling pathways

机译：维格列汀对大鼠鱼藤酮帕金森病模型的神经保护作用：RAGE-NFκB和Nrf2抗氧化信号通路的作用

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Gliptins have been recently shown to conquer neuronal degeneration in cell cultures via modulating glucagon-like peptide (GLP)-1. This peptide produced in the gut not only crosses the blood-brain barrier but is also synthesized in the brain and acts on GLP-1R exerting central anti-inflammatory and antiapoptotic effects, thus impeding neuronal damage. This study investigated the antiparkinsonian effect of vildagliptin, a dipeptidyl peptidase (DPP)-4 inhibitor in a rat rotenone model targeting mainly the RAGE-NFB/Nrf2-signaling pathways, to judge the potential anti-inflammatory/antioxidant effects of the drug. Vildagliptin markedly improved the motor performance in the open field and rotarod tests, effects that were emphasized by the accompanied reduction in striatal dopamine content. It modified the striatal energy level (ADP/ATP) associated with partial antagonism of body weight reduction. This incretin enhancer suppressed nuclear factor (NF)B and, consequently, the downstream inflammatory mediator tumor necrosis factor-. Normalization of receptor for advanced glycated end product (RAGE) is a main finding which justifies the anti-inflammatory effects of vildagliptin, together with hampering striatal inducible nitric oxide synthase, intracellular adhesion molecule-1 as well as myeloperoxidase. The antioxidant potential of vildagliptin was depicted as entailing reduction in thiobarbituric acid-reactive substances and the transcriptional factor Nrf-2 level. Vildagliptin guarded against neuronal demise through an antiapoptotic effect as reflected by the reduction in the mitochondrial matrix component cytochrome c and the key downstream executioner caspase-3. In conclusion, vildagliptin is endowed with various neuroprotective effects and thus can be a promising candidate for the management of Parkinson's disease.
机译：最近显示，脂蛋白可通过调节胰高血糖素样肽（GLP）-1征服细胞培养物中的神经元变性。肠道中产生的这种肽不仅穿过血脑屏障，而且还在大脑中合成，并作用于GLP-1R，发挥中枢抗炎和抗凋亡作用，从而阻止神经元损伤。这项研究调查了维达列汀（一种二肽基肽酶（DPP）-4抑制剂）在大鼠鱼藤酮模型中的抗帕金森病作用，该模型主要针对RAGE-NFB / Nrf2信号通路，以判断该药物的潜在抗炎/抗氧化作用。维达列汀在野外试验和轮转试验中显着改善了运动表现，伴随纹状体多巴胺含量降低而增强了这种效果。它改变了与体重减轻的部分拮抗作用有关的纹状体能级（ADP / ATP）。该肠降血糖素增强剂抑制了核因子（NF）B，并因此抑制了下游炎症介质肿瘤坏死因子-。晚期糖基化终产物（RAGE）受体的标准化是一个主要发现，证明维格列汀具有抗炎作用，并能抑制纹状体诱导型一氧化氮合酶，细胞内粘附分子1以及髓过氧化物酶。维格列汀的抗氧化潜力被描绘为需要降低硫代巴比妥酸反应性物质和转录因子Nrf-2的水平。维达列汀通过抗凋亡作用来预防神经元死亡，这反映在线粒体基质成分细胞色素c和关键下游执行者caspase-3减少上。总之，维格列汀具有多种神经保护作用，因此可以成为治疗帕金森氏病的有前途的候选药物。

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