2′,3′-Dideoxycytidine, a DNA Polymerase-β Inhibitor, Reverses Memory Deficits in a Mouse Model of Alzheimer’s Disease

Lysophosphatidic Acid Induces Apoptosis of PC12 Cells Through LPA1 Receptor/LPA2 Receptor/MAPK Signaling Pathway

“…The cells were differentiated by incubation in DMEM medium supplemented with 50 ng/ml nerve growth factor for 2 days before experiments. Primary rat cortical neurons were prepared from E16 embryos, and cultured as previously described (Liu et al, 2008;Meng et al, 2019) at 37 • C at 37 • C in a 5% CO 2 humidified incubator. Cortical neurons were cultured for 8 days in vitro before experiments.…”

The active components of Erzhi wan and their anti-Alzheimer's disease mechanisms determined by an integrative approach of network pharmacology, bioinformatics, molecular docking, and molecular dynamics simulation

“…This is consistent with the findings that oxidative stress induced DNA damage would lead to cognitive impairment in AD patients, which manifests the neuroprotective role of POLB [ 108 ]. However, inhibition of POLB through small molecules can reduce neuron death against Aβ neurotoxicity in vitro and in vivo studies [ 109 , 110 ]. This dilemma might be reconciled by the discovery that POLB is implicated with the Aβ induced cell cycle reentry, and ensuing neuronal apoptosis [ 111 , 112 ].…”

The LPA-CDK5-Tau Pathway Mediates Neuronal Injury in an In Vitro Model of Ischemia-Reperfusion Insult

“…SY5Y cells were cultured at 37°C in a 5% CO2/95% air atmosphere from CCFTCC. Mouse cortical neurons from Wt embryos, according to the previous description [24,25] , were cultured at 37°C in a 5% CO 2 incubator for 10 days. Treatment: Cortical neurons were treated with LPA (0, 4, 8, and 12 µM) for 4 h; DMSO (0.5 µM), LPA1 receptor inhibitor (0.5 µM), LPA2 receptor inhibitor (0.05 µM) and CDK5 inhibitor (0.5 µM) were added for a 2 h pretreatment, and then LPA (8 uM/L) was added for a 4 h treatment.…”