Citicoline (sodium)

Citicoline sodium is an endogenous intermediate in the synthesis of phosphatidylcholine which is a component of cell membranes. Citicoline sodium inhibits reactive oxygen species (ROS) and apoptosis. Citicoline sodium can be used for neurological disease and hearing loss study^[1][2][3]. In Vitro: Citicoline (1-100 μM, 24 h or 24 h before glutamate treatment) sodium increases rats retinal cells viability after glutamate-induced excitotoxicity, and has synergistic effects with Tramiprosate (Homotaurine) (HY-14602)^[1].
Citicoline (100 μM, 24 h before glutamate treatment and 30 min before HG treatment) sodium decreases proapoptotic effects associated with neuroretinal degeneration such as glutamate-induced excitotoxicity and high glucose (HG)-induced neurotoxicity, and has synergistic effects with Tramiprosate in rats retinal cells^[1].
Citicoline (100 μM, 36-48 h) sodium reduces apoptosis in mice cochlear hair cells (HCs) and HEI-OC-1 cells after Neomycin (HY-150520) exposure, decreases the mRNA level of pro-apoptotic factor and increases anti-apoptotic factor, suppresses proapoptotic protein expression^[2][3].
Citicoline (100 μM, 36-48 h) sodium attenuates oxidative stress in mice cochlear HCs and HEI-OC-1 cells after Neomycin injury^[3].
In Vivo: Citicoline (500-1000 mg/kg; i.p.; 1 h before test) sodium produces an anticonvulsant effect in pentylenetetrazole induced convulsion in male C57Bl/6 mice^[2].