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Liu et al. Journal of Neuroinflammation 2014, 11:47 http://jneuroinflammation/content/11/1/JOURNAL OF NEUROINFLAMMATIONRESEARCHOpen AccessParoxetine ameliorates lipopolysaccharide-induced microglia activation by way of differential regulation of MAPK signalingRong-Pei Liu1, Ming Zou1, Jian-Yong Wang1, Juan-Juan Zhu1, Jun-Mei Lai1, Li-Li Zhou1, Song-Fang Chen1, Xiong Zhang1* and Jian-Hong Zhu1,2*AbstractBackground: Paroxetine, a selective serotonin reuptake inhibitor for counteracting depression, has been recently suggested as obtaining a part in prevention of dopaminergic neuronal degeneration in substantia nigra, a hallmark of Parkinson’s disease (PD).1-Methylcyclopropaneacetic acid web The pathogenesis of this type of neurological issues often involves the activation of microglia and connected inflammatory processes. Therefore in this study we aimed to know the part of paroxetine in microglia activation and to elucidate the underlying mechanism(s).Metformin web Approaches: BV2 and main microglial cells were pretreated with paroxetine and stimulated with lipopolysaccharide (LPS).PMID:35126464 Cells have been assessed for the responses of pro-inflammatory mediator and cytokines, along with the connected signaling pathways have been evaluated and analyzed in BV2 cells. Results: Paroxetine significantly inhibited LPS-induced production of nitric oxide (NO) and pro-inflammatory cytokines for example TNF- and IL-1. Additional analysis showed inducible nitric oxide synthase (iNOS) and mRNA expression of TNF- and IL-1 have been attenuated by paroxetine pretreatment. Analyses in signaling pathways demonstrated that paroxetine led to suppression of LPS-induced JNK1/2 activation and baseline ERK1/2 activity, but had little impact on the activation of p38 and p65/NF-B. Interference with precise inhibitors revealed that paroxetine-mediated suppression of NO production was via JNK1/2 pathway whilst the cytokine suppression was by way of both JNK1/2 and ERK1/2 pathways. In addition, conditioned media culture showed that paroxetine suppressed the microglia-mediated neurotoxicity. Conclusions: Paroxetine inh.
