TY - JOUR A2 - 门多萨少年，旧金山海梅B. AU - 辛格，森Saumitra AU - 清莱，Sachchida的Nand AU - 贝拉，Hareram AU - 扎赫拉，瓦利亚AU - 拉索，Aaina辛格AU - Dilnashin，Hagera AU - 辛格，RichaAU - 辛格，苏里亚普拉塔普PY - 2020 DA - 2020年5月27日TI - 对多巴胺神经元的线粒体功能障碍介导的细胞凋亡死亡绿原酸的保护作用在帕金森病小鼠模型SP - 6571484 VL - 2020 AB - 线粒体功能障碍和氧化stress characterize major factors involved in the activation of complex processes corresponding to apoptosis-mediated neuronal senescence of dopaminergic neurons (DA) in Parkinson’s disease (PD). Here, we evaluated the molecular mechanisms participating in the treatment of a 1-methyl-4-phenyl-1,2,3,6-tetrahydopyridine- (MPTP-) intoxicated PD mouse model in response to chlorogenic acid (CGA). The results indicate that CGA treatment significantly improved the motor coordination of the MPTP-intoxicated mice. CGA also alleviated the fall in activity of mitochondrial complexes I, IV, and V in accordance with ameliorating the level of superoxide dismutase and mitochondrial glutathione in the midbrain of MPTP-induced mice. CGA inhibited the activation of proapoptotic proteins including Bax and caspase-3, while elevating the expression of antiapoptotic protein like Bcl-2 consequently preventing the MPTP-mediated apoptotic cascade. The study also revealed the improved phosphorylation state of Akt, ERK1/2, and GSK3 β其下调如MPTP毒性的效果。我们的研究结果表明该CGA可具有药理学性质，并与GSK3磷酸化相关联的PD小鼠模型有助于打击MPTP诱导的毒性的神经保护 β通过激活的Akt / ERK在线粒体内在凋亡途径的信号。因此，CGA治疗可以作为用于在PD DA神经元的线粒体介导的凋亡衰老的潜在治疗候选产生。SN - 1942-0900 UR - https://doi.org/10.1155/2020/6571484 DO - 10.1155 /六百五十七万一千四百八十四分之二千○二十〇JF - 氧化医学和细胞寿命PB - Hindawi出版KW - ER -