The effect of Piper laetispicum extract (EAE-P) during chronic unpredictable mild stress based on interrelationship of inflammatory cytokines, apoptosis cytokines and neurotrophin in the hippocampus

Xie, Hui; Jin, Di; Kang, Yubin; Shi, Xueru; Liu, Hongrui; Shen, Haixing; Chen, Jian; Yan, Macheng; Liu, Juan; Pan, Shengli

doi:10.1186/s12906-015-0747-8

Cited by 14 publications

(14 citation statements)

References 31 publications

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“…In particular, in line with the literature and our hypothesis, treatment in a stressful condition overall led to an anti-inflammatory response (Cheng et al, 2016;Ji et al, 2014;Jiang et al, 2013;Lu et al, 2014;Tianzhu et al, 2014;Wilson et al, 2014;Xie et al, 2015). By contrast, fluoxetine treatment in an enriched condition led to an increased expression of inflammatory genes.…”

Section: Resultssupporting

confidence: 91%

“…These findings indicate that fluoxetine increases the overall inflammatory milieu in the enriched condition, while exerting an opposite effect in the stressful condition. The latter result is in line with previous studies showing that fluoxetine, when administered to mice exposed to a stressful environment, overall reduces hippocampal expression of pro-inflammatory cytokines (Cheng et al, 2016;Ji et al, 2014;Jiang et al, 2013;Lu et al, 2014;Tianzhu et al, 2014;Wilson et al, 2014;Xie et al, 2015).…”

Section: Fluoxetine Affects Hippocampal Inflammatory Mediatorssupporting

confidence: 92%

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Fluoxetine treatment affects the inflammatory response and microglial function according to the quality of the living environment

Alboni

Poggini

Garofalo

et al. 2016

Brain, Behavior, and Immunity

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It has been hypothesized that selective serotonin reuptake inhibitors (SSRIs), the most common treatment for major depression, affect mood through changes in immune function. However, the effects of SSRIs on inflammatory response are contradictory since these act either as anti-or pro-inflammatory drugs. Previous experimental and clinical studies showed that the quality of the living environment moderates the outcome of antidepressant treatment. Therefore, we hypothesized that the interplay between SSRIs and the environment may, at least partially, explain the apparent incongruence regarding the effects of SSRI treatment on the inflammatory response. In order to investigate such interplay, we exposed C57BL/6 mice to chronic stress to induce a depression-like phenotype and, subsequently, to fluoxetine treatment or vehicle (21days) while being exposed to either an enriched or a stressful condition. At the end of treatment, we measured the expression levels of several anti-and pro-inflammatory cytokines and inflammatory mediators in the whole hippocampus and in isolated microglia. We also determined microglial density, distribution, and morphology to investigate their surveillance state. Results show that the effects of fluoxetine treatment on inflammation and microglial function, as compared to vehicle, were dependent on the quality of the living environment. In particular, fluoxetine administered in the enriched condition increased the expression of pro-inflammatory markers compared to vehicle, while treatment in a stressful condition produced anti-inflammatory effects. These findings provide new insights regarding the effects of SSRIs on inflammation, which may be crucial to devise pharmacological strategies aimed at enhancing antidepressant efficacy by means of controlling environmental conditions. AbstractIt has been hypothesized that selective serotonin reuptake inhibitors (SSRIs), the most common treatment for major depression, affect mood through changes in immune function. However, the effects of SSRIs on inflammatory response are contradictory since these drugs act either as anti-or proinflammatory. Previous experimental and clinical studies showed that the quality of the living environment moderates the outcome of antidepressant treatment. Therefore, we hypothesized that the interplay between SSRIs and environment may, at least partially, explain the apparent incongruence regarding the effects of SSRI treatment on the inflammatory response. In order to investigate such interplay, we exposed C57BL/6 mice to chronic stress to induce a depression-like phenotype and, subsequently, to fluoxetine treatment or vehicle (21 days) while being exposed to either an enriched or a stressful condition. At the end of treatment, we measured the expression levels of several anti-and pro-inflammatory cytokines and inflammatory mediators in the whole hippocampus and in isolated microglia. We also determined microglial density, distribution, and morphology to investigate their surveillance state. Results show that...

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Section: Resultssupporting

confidence: 91%

Section: Fluoxetine Affects Hippocampal Inflammatory Mediatorssupporting

confidence: 92%

Fluoxetine treatment affects the inflammatory response and microglial function according to the quality of the living environment

Alboni

Poggini

Garofalo

et al. 2016

Brain, Behavior, and Immunity

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“…Each of these models entails different mechanisms, such as changes in kynurenine metabolites, altered neurotransmitter signaling, and others [21, 36]. Additionally, some similarities such as alterations in cytokines and BDNF levels are also observed in most models, mimicking observations recorded in psychiatric patients [37, 39, 40].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Brain Cytokines and the Level of Brain-Derived Neurotrophic Factor in an Inflammatory Model of Depression

Horita

Silva

Ferrari

et al. 2020

Neuroimmunomodulation

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Introduction: Major depressive disorder is considered a global public health problem. Inflammatory processes are likely involved in its pathophysiology, but the underlying mechanisms have remained uncertain.Here, we used the model of systemic lipopolysaccharide (LPS) injection to test the hypothesis that depressive-like behaviors occur along with changes in the levels of cytokines and brain-derived neurotrophic factor (BDNF) in the hippocampus (HC), prefrontal cortex (PFC), and hypothalamus (HT), and can be prevented by dexamethasone administration. Methods: Adult C57Bl/6 male mice were first isolated for 10 days, and thereafter received an injection of dexamethasone (6 mg/kg, intraperitoneal [i.p.]), saline followed by LPS (0.83 mg/kg, i.p.), or saline. After 6 h, animals were subjected to the forced-swim test (FST) and open-field tests. Immediately after the behavioral tests, they were euthanized and their brains were collected for the biochemical analyses. Results: LPS increased the immobility time and reduced the distance travelled in the FST and open-field test, respectively. Dexamethasone increased the immobility time in saline-treated mice but reduced this behavior in the LPS group. LPS increased the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6 and interferon (IFN)-γ in most of the regions evaluated. Dexamethasone prevented LPS-induced IL-6 in the HC, PFC, and HT. Interestingly, dexamethasone increased IL-4 and IL-10 levels in both the LPS- and saline-treated groups. Although dexamethasone reduced BDNF in saline-treated mice, it prevented LPS-induced reduction in this neurotrophic factor. Conclusion: In summary, dexamethasone decreased proinflammatory and increased anti-inflammatory levels of cytokines and prevented a reduction in BDNF levels induced by the inflammatory stimulus. Thus, the attenuation of depressive-like behavior induced by dexamethasone may be related to the effects on these parameters.

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“…Anti-inflammatory agents may be a useful antidepressant therapy or an adjuvant to the currently available conventional therapies (20). Mice exposed to CUMS significantly enhanced the productions of TNF-a and IL-6 in the hippocampus, and these changes could be reversed by treatment with antidepressant therapy (46). The results of our present study also demonstrated that CUMS treatment significantly enhanced the levels of TNF-a and IL-6 in the hippocampus and cerebral cortex of the mice, whereas treatment with IRN could restore the release of TNF-a and IL-6 induced by CUMS.…”

Section: Discussionmentioning

confidence: 99%

Isorhynchophylline exerts antidepressant‐like effects in mice via modulating neuroinflammation and neurotrophins: involvement of the PI3K/Akt/GSK‐3β signaling pathway

Xian

et al. 2019

FASEB j.

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Isorhynchophylline (IRN), an oxindole alkaloid isolated from Uncaria rhynchophylla, elicited distinct antidepressant‐like activity in mice. The present study aimed to investigate the antidepressant‐like effects of IRN in chronic unpredictable mild stress (CUMS)‐induced depressive‐like behaviors in mice and to illustrate its possible mechanisms of action. The mice were subjected to CUMS for 6 wk and administered with IRN (20 or 40 mg/kg) daily by oral gavage for 3 wk. The PI3K/protein kinase B (Akt) inhibitor and glycogen synthase kinase‐3β (GSK‐3β) inhibitors were used to determine the involvement of the PI3K/Akt/GSK‐3β pathway in the antidepressant‐like effects of IRN in the mice. The results showed that CUMS caused depression‐like behaviors in the mice, such as behavioral despair by the forced swim test (FST) and anhedonia by the sucrose preference test. In addition, CUMS could significantly reduce the levels of nerve growth factor and brain‐derived neurotrophic factor but markedly increase the release of TNF‐α and IL‐6 in the hippocampus and cerebral cortex of the mice. Western blotting analysis showed that CUMS markedly suppressed the levels of phosphorylated GSK‐3β (Ser9) and phosphorylated Akt (Ser473) but significantly enhanced the translocation of NF‐κB p65 from cytosol to nuclei in the hippocampus and cerebral cortex of the mice. CUMS could also significantly increase the NF‐κB binding activity in the hippocampus and cerebral cortex of the mice, whereas IRN treatment could significantly reverse the behavioral and biochemical changes induced by CUMS in the mice. Moreover, the antidepressant‐like effect of IRN was completely abolished by the PI3K/Akt inhibitor. Combination treatment with IRN and GSK‐3β inhibitors in the mice exerted a synergistic anti‐immobility action in the FST. The results of mechanistic investigations indicated that the antidepressant‐like action of IRN was mediated, at least in part, by enhancing neurotrophins and attenuating neuroinflammation via modulating the PI3K/Akt/GSK‐3β pathway.—Xian, Y.‐F., Ip, S.‐P., Li, H.‐Q., Qu, C., Su, Z.‐R., Chen, J.‐N., Lin, Z.‐X. Isorhynchophylline exerts antidepressant‐like effects in mice via modulating neuroinflammation and neurotrophins: involvement of the PI3K/Akt/GSK‐3β signaling pathway. FASEB J. 33, 10393–10408 (2019). http://www.fasebj.org

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The effect of Piper laetispicum extract (EAE-P) during chronic unpredictable mild stress based on interrelationship of inflammatory cytokines, apoptosis cytokines and neurotrophin in the hippocampus

Cited by 14 publications

References 31 publications

Fluoxetine treatment affects the inflammatory response and microglial function according to the quality of the living environment

Fluoxetine treatment affects the inflammatory response and microglial function according to the quality of the living environment

Evaluation of Brain Cytokines and the Level of Brain-Derived Neurotrophic Factor in an Inflammatory Model of Depression

Isorhynchophylline exerts antidepressant‐like effects in mice via modulating neuroinflammation and neurotrophins: involvement of the PI3K/Akt/GSK‐3β signaling pathway

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