Oxytocin inhibits lipopolysaccharide-induced inflammation in microglial cells and attenuates microglial activation in lipopolysaccharide-treated mice

Yuan, Lin; Liu, Song; Bai, Xuemei; Gao, Yan; Liu, Guangheng; Wang, Xueer; Liu, Dexiang; Li, Tong; Hao, Aijun; Wang, Zhen

doi:10.1186/s12974-016-0541-7

Cited by 160 publications

(156 citation statements)

References 52 publications

(71 reference statements)

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“…The GluN2B subunit of NMDA receptors is thought to exert a main channel function in the brain . Activation of NMDA receptors, including the GluN2B subunit, induces Ca 2+ influx, thus augmenting intracellular Ca 2+ levels and activating CaMKs . In the present study, we observed that ketamine reduced LPS‐induced Ca 2+ levels and CaMK II phosphorylation, thus inhibiting LPS‐mediated inflammation in BV2 cells.…”

Section: Discussionsupporting

confidence: 63%

Ketamine inhibits LPS‐mediated BV2 microglial inflammation via NMDA receptor blockage

Ding

et al. 2019

Fundamemntal Clinical Pharma

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Microglial inflammation leads to the upregulation of proinflammatory cytokine and proinflammatory enzyme expression, resulting in inflammation‐induced neuronal cell apoptosis. Ketamine, an anesthetic mostly used in critical patients, has been reported to possess neuroprotective effects. However, the potential mechanism is still not well understood. In the present study, we investigated how ketamine attenuates lipopolysaccharide (LPS)‐mediated BV2 cell inflammation. LPS upregulated proinflammatory cytokine and proinflammatory enzyme expression, increased NF‐κB phosphorylation and nuclear translocation, and augmented calcium (Ca2+)/calmodulin‐dependent protein kinase II (CaMK II) phosphorylation and Ca2+ levels in BV2 cells. Ketamine could reverse these LPS‐induced effects. Furthermore, AP5, an inhibitor of NMDA receptors, inhibited LPS‐induced inflammatory effects in BV2 cells, which was similar to the effects of ketamine. Moreover, these effects of ketamine against LPS‐mediated inflammation in BV2 cells could be reversed by D‐serine, an activator of NMDA receptors. The present study suggests that ketamine, by inhibiting NMDA receptors, attenuating Ca2+ levels, and inhibiting CaMK II phosphorylation, NF‐κB phosphorylation and nuclear translocation, may ameliorate LPS‐mediated inflammation in BV2 cells.

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Section: Discussionsupporting

confidence: 63%

Ketamine inhibits LPS‐mediated BV2 microglial inflammation via NMDA receptor blockage

Ding

et al. 2019

Fundamemntal Clinical Pharma

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“…Prolactin has been found to enhance the inflammatory response and proliferation of glia following a traumatic brain injury (Möderscheim et al, 2007), and oxytocin administration has been found to alleviate tissue damage in various animal models of injury (Akdemir et al, 2014; Houshmand et al, 2009; Karelina et al, 2011). The protective mechanisms by which prolactin and oxytocin act may be related to a decrease in pro-inflammatory cytokines from microglia, macrophages, and endothelial cells (Akman et al, 2015; Szeto et al, 2008; Tug˘tepe et al, 2013; Yuan et al, 2016). …”

Section: Discussionmentioning

confidence: 99%

An examination of changes in maternal neuroimmune function during pregnancy and the postpartum period

Sherer

Posillico

Schwarz

2017

Brain, Behavior, and Immunity

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There is strong evidence that the immune system changes dramatically during pregnancy in order to prevent the developing fetus from being "attacked" by the maternal immune system. Due to these alterations in peripheral immune function, many women that suffer from autoimmune disorders actually find significant relief from their symptoms throughout pregnancy; however, these changes can also leave the mother more susceptible to infections that would otherwise be mitigated by the inflammatory response (Robinson and Klein, 2012). Only one other study has looked at changes in microglial number and morphology during pregnancy and the postpartum period (Haim et al., 2016), but no one has yet examined the neuroimmune response following an immune challenge during this time. Therefore, in this study, we investigated the impact of an immune challenge during various time-points throughout pregnancy and the postpartum period on the expression of immune molecules in the brain of the mother and fetus. Our results indicate that similar to the peripheral immune suppression measured during pregnancy, we also see significant suppression of the immune response in the maternal brain, particularly during late gestation. In contrast to the peripheral immune system, immune modulation in the maternal brain extends moderately into the postpartum period. Additionally, we found that the fetal immune response in the brain and placenta is also suppressed just before parturition, suggesting that cytokine production in the fetus and placenta are mirroring the peripheral cytokine response of the mother.

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“…In general, microglia play an important role in neuroprotection, especially confrontation with pathogens from the external environment; however, overexpression of microglia causes many key cellular responses that can cause diseases by inducing pro-inflammatory mediators such as NO, PGE 2 and TNF-α (Lee et al, 2011). Therefore, a promising therapeutic strategy used for neurodegenerative diseases was focused on blocking microglial activation processes (Kim and Joh, 2006;Yuan et al, 2016). Recently, numerous studies have reported that traditional Chinese medicine exert neuroprotective effects through suppressing microglial activation, and their effects have been elevated to have the potential to treat neurodegenerative diseases Wang et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Endoplasmic Reticulum Stress and NF-κB Pathway in Salidroside Mediated Neuroprotection: Potential of Salidroside in Neurodegenerative Diseases

Wang

Lou

et al. 2017

Am. J. Chin. Med.

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Microglial activation leads to increased production of proinflammatory enzymes and cytokines, which is considered to play crucial role in neurodegenerative diseases, however there are only a few drugs that target microglia activation. Recent studies have indicated that the Traditional Chinese Medicine, salidroside (Sal), exerted anti-inflammatory effects. According to this evidence, our present study aims to explore the effect of the Sal (a phenylpropanoid glycoside compound which is isolated from rhodiola), on microglia activation in lipopolysaccharide (LPS)-stimulated BV-2 cells. Our results showed that Sal could significantly inhibit the excessive production of Nitric Oxide (NO) and Prostaglandin E2 (PGE 2 ) in LPS-stimulated BV2 cells. Moreover, Sal treatment could suppress the mRNA and protein expressions of inflammatory enzymes, including Inducible Nitric Oxide Synthase (iNOS) and Cyclooxygenase-2 (COX-2). The mechanisms may be related to the inhibition of the activation of Nuclear Factor-kappaB (NF-κB) and endoplasmic reticulum stress. Our study demonstrated that salidroside could inhibit lipopolysaccharide-induced microglia The American Journal of Chinese Medicine, Vol. 45, No. 7, 1459-1475 © 2017 activation via the inhibition of the NF-κB pathway and endoplasmic reticulum stress, which makes it a promising therapeutic agent for human neurodegenerative diseases.

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Oxytocin inhibits lipopolysaccharide-induced inflammation in microglial cells and attenuates microglial activation in lipopolysaccharide-treated mice

Cited by 160 publications

References 52 publications

Ketamine inhibits LPS‐mediated BV2 microglial inflammation via NMDA receptor blockage

Ketamine inhibits LPS‐mediated BV2 microglial inflammation via NMDA receptor blockage

An examination of changes in maternal neuroimmune function during pregnancy and the postpartum period

Endoplasmic Reticulum Stress and NF-κB Pathway in Salidroside Mediated Neuroprotection: Potential of Salidroside in Neurodegenerative Diseases

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