Antidepressant-like effects of curcumin in chronic mild stress of rats: Involvement of its anti-inflammatory action

Jiang, Hong; Wang, Zhen; Wang, Yihe; Xie, Kai; Zhang, Qingrui; Luan, Qinsong; Chen, Wenqiang; Liu, Dexiang

doi:10.1016/j.pnpbp.2013.07.009

Cited by 96 publications

(48 citation statements)

References 42 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: 90%

“…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: 90%

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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“…Exploratory analyses on people with atypical depression were also conducted, and several questionnaires were used to assess depressive, anxiety and general health changes. Further support for the antidepressant effects of curcumin is provided by consistent findings of protective behavioural effects in animal models of depression and chronic mild stress (Jiang et al, 2013, Sanmukhani et al, 2011, Zhang et al, 2014). …”

Section: Discussionmentioning

confidence: 91%

Curcumin for the treatment of major depression: A randomised, double-blind, placebo controlled study

Lopresti

Maes

Maker

et al. 2014

Journal of Affective Disorders

172

100

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“…Antidepressant treatment attenuates the expression of inflammatory cytokines and depression‐like behavior of the stressed rats (Jiang et al., 2013; Rossetti et al., 2016). Based on these findings, inflammation may play a central role in the induction of a depressive phenotype.…”

Section: Discussionmentioning

confidence: 99%

Gunn rats with glial activation in the hippocampus show prolonged immobility time in the forced swimming test and tail suspension test

et al. 2018

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IntroductionRecent studies imply that glial activation plays a role in the pathogenesis of psychiatric disorders, such as schizophrenia and major depression. We previously demonstrated that Gunn rats with hyperbilirubinemia show congenital gliosis and schizophrenia‐like behavior.MethodsAs it has been suggested that major depression involves glial activation associated with neuroinflammation, we examined whether Gunn rats show depression‐like behavior using the forced swimming test (FST) and the tail suspension test (TST). In addition, we quantitatively evaluated both microgliosis and astrogliosis in the hippocampus of Gunn rats using immunohistochemistry analysis of the microglial marker ionized calcium‐binding adaptor molecule (Iba) 1 and the astrocytic marker S100B.ResultsBoth the FST and TST showed that immobility time of Gunn rats was significantly longer than that of normal control Wistar rats, indicating that Gunn rats are somewhat helpless, a sign of depression‐like behavior. In the quantification of immunohistochemical analysis, Iba1immunoreactivity in the dentate gyrus (DG), cornu ammonis (CA) 1, and CA3 and the number of Iba1‐positive cells in the CA1 and CA3 were significantly increased in Gunn rats compared to Wistar rats. S100B immunoreactivity in the DG, CA1, and CA3 and the number of S100B‐positive cells in the DG and CA3 were significantly increased in Gunn rats compared to Wistar rats.ConclusionOur findings suggest that both microglia and astrocyte are activated in Gunn rats and their learned helplessness could be related to glial activation.

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Antidepressant-like effects of curcumin in chronic mild stress of rats: Involvement of its anti-inflammatory action

Cited by 96 publications

References 42 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

Curcumin for the treatment of major depression: A randomised, double-blind, placebo controlled study

Gunn rats with glial activation in the hippocampus show prolonged immobility time in the forced swimming test and tail suspension test

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