Modi Jigar Pravinchandra, Shen Wen, Menzie-Suderam Janet, Xu Hongyuan, Lin Chun-Hua, Tao Rui, Prentice Howard M, Schloss John, Wu Jang-Yen
Department of Biomedical Sciences, Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL 33431, USA.
Center of Complex Systems and Brain Sciences, Florida Atlantic University, Boca Raton, FL 33431, USA.
Biomedicines. 2023 Jul 3;11(7):1885. doi: 10.3390/biomedicines11071885.
Carbamathione (Carb), an NMDA glutamate receptor partial antagonist, has potent neuroprotective functions against hypoxia- or ischemia-induced neuronal injury in cell- or animal-based stroke models. We used PC-12 cell cultures as a cell-based model and bilateral carotid artery occlusion (BCAO) for stroke. Whole-cell patch clamp recording in the mouse retinal ganglion cells was performed. Key proteins involved in apoptosis, endoplasmic reticulum (ER) stress, and heat shock proteins were analyzed using immunoblotting. Carb is effective in protecting PC12 cells against glutamate- or hypoxia-induced cell injury. Electrophysiological results show that Carb attenuates NMDA-mediated glutamate currents in the retinal ganglion cells, which results in activation of the AKT signaling pathway and increased expression of pro-cell survival biomarkers, e.g., Hsp 27, P-AKT, and Bcl2 and decreased expression of pro-cell death markers, e.g., Beclin 1, Bax, and Cleaved caspase 3, and ER stress markers, e.g., CHOP, IRE1, XBP1, ATF 4, and eIF2α. Using the BCAO animal stroke model, we found that Carb reduced the brain infarct volume and decreased levels of ER stress markers, GRP 78, CHOP, and at the behavioral level, e.g., a decrease in asymmetric turns and an increase in locomotor activity. These findings for Carb provide promising and rational strategies for stroke therapy.
卡巴谷胱甘肽(Carb)是一种N-甲基-D-天冬氨酸(NMDA)谷氨酸受体部分拮抗剂,在基于细胞或动物的中风模型中,对缺氧或缺血诱导的神经元损伤具有强大的神经保护功能。我们使用PC-12细胞培养物作为基于细胞的模型,并采用双侧颈动脉闭塞(BCAO)来模拟中风。对小鼠视网膜神经节细胞进行了全细胞膜片钳记录。使用免疫印迹法分析了参与细胞凋亡、内质网(ER)应激和热休克蛋白的关键蛋白。Carb可有效保护PC12细胞免受谷氨酸或缺氧诱导的细胞损伤。电生理结果表明,Carb可减弱视网膜神经节细胞中NMDA介导的谷氨酸电流,从而激活AKT信号通路,并增加细胞存活促进生物标志物(如热休克蛋白27、磷酸化AKT和Bcl2)的表达,同时降低细胞死亡标志物(如Beclin 1、Bax和裂解的半胱天冬酶3)以及内质网应激标志物(如CHOP、IRE1、XBP1、ATF 4和eIF2α)的表达。使用BCAO动物中风模型,我们发现Carb可减少脑梗死体积,并降低内质网应激标志物葡萄糖调节蛋白78(GRP 78)、CHOP的水平,在行为水平上,例如减少不对称转弯并增加运动活动。这些关于Carb的发现为中风治疗提供了有前景且合理的策略。