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The mechanism of antidepressant action of escitalopram, the S-enantiomer of racemic citalopram, is presumed to be linked to potentiation of serotonergic activity in the central nervous system (CNS) resulting from its inhibition of CNS neuronal reuptake of serotonin (5-HT)

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While LPS stimulation increases the G0/G1 phase and decreases the G2/M phase, pterostilbene treatment shortened the G0/G1 phase and prolonged the G2/M phase