Ladostigil Attenuates Induced Oxidative Stress in Human Neuroblast-like SH-SY5Y Cells

A hallmark of the aging brain is robust inflammation mediated by microglial activation. Pathophysiology common neurodegenerative diseases involves oxidative stress and neuroinflammation. Chronic treatment rats ladostigil, a compound with antioxidant anti-inflammatory function, prevented activation learning deficits. In this study, we further investigate effect ladostigil on undifferentiated SH-SY5Y cells. We show that cells exposed to acute (by H2O2) or chronic Sin1, 3-morpholinosydnonimine) induced apoptotic cell death. However, in presence decline viability increase levels were partially reversed. RNA-seq analysis showed prolonged oxidation Sin1 resulted simultaneous reduction expression level endoplasmic reticulum (ER) genes participate proteostasis. By comparing differential gene profile treated incubated before being observed an over-expression Clk1 (Cdc2-like kinase 1) which was implicated psychophysiological mice Alzheimer’s disease. Ladostigil also suppressed Ccpg1 (Cell cycle progression Synj1 (Synaptojanin are involved ER-autophagy endocytic pathways. postulate alleviated damage oxidation. Therefore, under conditions brain, may block processes consequently reduce neurotoxicity.