Risperidone significantly inhibits interferon-γ-induced microglial activation in vitro

Takahiro Kato, Akira Monji, Sadayuki Hashioka, Shigenobu Kanba

Research output: Contribution to journalArticle

127 Citations (Scopus)

Abstract

Microglia has recently been regarded to be a mediator of neuroinflammation via the release of proinflammatory cytokines, nitric oxide (NO) and reactive oxygen species (ROS) in the central nervous system (CNS). Microglia has thus been reported to play an important role in the pathology of neurodegenerative disease, such as Alzheimer's disease (AD) and Parkinson's disease (PD). The pathological mechanisms of schizophrenia remain unclear while some recent neuroimaging studies suggest even schizophrenia may be a kind of neurodegenerative disease. Risperidone has been reported to decrease the reduction of MRI volume during the clinical course of schizophrenia. Many recent studies have demonstrated that immunological mechanisms via such as interferon (IFN)-γ and cytokines might be relevant to the pathophysiology of schizophrenia. In the present study, we thus investigated the effects of risperidone on the generation of nitric oxide, inducible NO synthase (iNOS) expression and inflammatory cytokines: interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α by IFN-γ-activated microglia by using Griess assay, Western blotting and ELISA, respectively. In comparison with haloperidol, risperidone significantly inhibited the production of NO and proinflammatory cytokines by activated microglia. The iNOS levels of risperidone-treated cells were much lower than those of the haloperidol-treated cells. Antipsychotics, especially risperidone may have an anti-inflammatory effect via the inhibition of microglial activation, which is not only directly toxic to neurons but also has an inhibitory effect on neurogenesis and oligodendrogenesis, both of which have been reported to play a crucial role in the pathology of schizophrenia.

Original languageEnglish
Pages (from-to)108-115
Number of pages8
JournalSchizophrenia research
Volume92
Issue number1-3
DOIs
Publication statusPublished - May 1 2007

Fingerprint

Risperidone
Interferons
Microglia
Schizophrenia
Cytokines
Nitric Oxide
Haloperidol
Neurodegenerative Diseases
Pathology
Poisons
Neurogenesis
Nitric Oxide Synthase Type II
Interleukin-1
Neuroimaging
Nitric Oxide Synthase
Antipsychotic Agents
Parkinson Disease
Interleukin-6
Reactive Oxygen Species
Alzheimer Disease

All Science Journal Classification (ASJC) codes

  • Psychiatry and Mental health
  • Biological Psychiatry

Cite this

Risperidone significantly inhibits interferon-γ-induced microglial activation in vitro. / Kato, Takahiro; Monji, Akira; Hashioka, Sadayuki; Kanba, Shigenobu.

In: Schizophrenia research, Vol. 92, No. 1-3, 01.05.2007, p. 108-115.

Research output: Contribution to journalArticle

Kato, Takahiro ; Monji, Akira ; Hashioka, Sadayuki ; Kanba, Shigenobu. / Risperidone significantly inhibits interferon-γ-induced microglial activation in vitro. In: Schizophrenia research. 2007 ; Vol. 92, No. 1-3. pp. 108-115.
@article{c330b65412d245958b89db0c51441182,
title = "Risperidone significantly inhibits interferon-γ-induced microglial activation in vitro",
abstract = "Microglia has recently been regarded to be a mediator of neuroinflammation via the release of proinflammatory cytokines, nitric oxide (NO) and reactive oxygen species (ROS) in the central nervous system (CNS). Microglia has thus been reported to play an important role in the pathology of neurodegenerative disease, such as Alzheimer's disease (AD) and Parkinson's disease (PD). The pathological mechanisms of schizophrenia remain unclear while some recent neuroimaging studies suggest even schizophrenia may be a kind of neurodegenerative disease. Risperidone has been reported to decrease the reduction of MRI volume during the clinical course of schizophrenia. Many recent studies have demonstrated that immunological mechanisms via such as interferon (IFN)-γ and cytokines might be relevant to the pathophysiology of schizophrenia. In the present study, we thus investigated the effects of risperidone on the generation of nitric oxide, inducible NO synthase (iNOS) expression and inflammatory cytokines: interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α by IFN-γ-activated microglia by using Griess assay, Western blotting and ELISA, respectively. In comparison with haloperidol, risperidone significantly inhibited the production of NO and proinflammatory cytokines by activated microglia. The iNOS levels of risperidone-treated cells were much lower than those of the haloperidol-treated cells. Antipsychotics, especially risperidone may have an anti-inflammatory effect via the inhibition of microglial activation, which is not only directly toxic to neurons but also has an inhibitory effect on neurogenesis and oligodendrogenesis, both of which have been reported to play a crucial role in the pathology of schizophrenia.",
author = "Takahiro Kato and Akira Monji and Sadayuki Hashioka and Shigenobu Kanba",
year = "2007",
month = "5",
day = "1",
doi = "10.1016/j.schres.2007.01.019",
language = "English",
volume = "92",
pages = "108--115",
journal = "Schizophrenia Research",
issn = "0920-9964",
publisher = "Elsevier",
number = "1-3",

}

TY - JOUR

T1 - Risperidone significantly inhibits interferon-γ-induced microglial activation in vitro

AU - Kato, Takahiro

AU - Monji, Akira

AU - Hashioka, Sadayuki

AU - Kanba, Shigenobu

PY - 2007/5/1

Y1 - 2007/5/1

N2 - Microglia has recently been regarded to be a mediator of neuroinflammation via the release of proinflammatory cytokines, nitric oxide (NO) and reactive oxygen species (ROS) in the central nervous system (CNS). Microglia has thus been reported to play an important role in the pathology of neurodegenerative disease, such as Alzheimer's disease (AD) and Parkinson's disease (PD). The pathological mechanisms of schizophrenia remain unclear while some recent neuroimaging studies suggest even schizophrenia may be a kind of neurodegenerative disease. Risperidone has been reported to decrease the reduction of MRI volume during the clinical course of schizophrenia. Many recent studies have demonstrated that immunological mechanisms via such as interferon (IFN)-γ and cytokines might be relevant to the pathophysiology of schizophrenia. In the present study, we thus investigated the effects of risperidone on the generation of nitric oxide, inducible NO synthase (iNOS) expression and inflammatory cytokines: interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α by IFN-γ-activated microglia by using Griess assay, Western blotting and ELISA, respectively. In comparison with haloperidol, risperidone significantly inhibited the production of NO and proinflammatory cytokines by activated microglia. The iNOS levels of risperidone-treated cells were much lower than those of the haloperidol-treated cells. Antipsychotics, especially risperidone may have an anti-inflammatory effect via the inhibition of microglial activation, which is not only directly toxic to neurons but also has an inhibitory effect on neurogenesis and oligodendrogenesis, both of which have been reported to play a crucial role in the pathology of schizophrenia.

AB - Microglia has recently been regarded to be a mediator of neuroinflammation via the release of proinflammatory cytokines, nitric oxide (NO) and reactive oxygen species (ROS) in the central nervous system (CNS). Microglia has thus been reported to play an important role in the pathology of neurodegenerative disease, such as Alzheimer's disease (AD) and Parkinson's disease (PD). The pathological mechanisms of schizophrenia remain unclear while some recent neuroimaging studies suggest even schizophrenia may be a kind of neurodegenerative disease. Risperidone has been reported to decrease the reduction of MRI volume during the clinical course of schizophrenia. Many recent studies have demonstrated that immunological mechanisms via such as interferon (IFN)-γ and cytokines might be relevant to the pathophysiology of schizophrenia. In the present study, we thus investigated the effects of risperidone on the generation of nitric oxide, inducible NO synthase (iNOS) expression and inflammatory cytokines: interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α by IFN-γ-activated microglia by using Griess assay, Western blotting and ELISA, respectively. In comparison with haloperidol, risperidone significantly inhibited the production of NO and proinflammatory cytokines by activated microglia. The iNOS levels of risperidone-treated cells were much lower than those of the haloperidol-treated cells. Antipsychotics, especially risperidone may have an anti-inflammatory effect via the inhibition of microglial activation, which is not only directly toxic to neurons but also has an inhibitory effect on neurogenesis and oligodendrogenesis, both of which have been reported to play a crucial role in the pathology of schizophrenia.

UR - http://www.scopus.com/inward/record.url?scp=34147102249&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34147102249&partnerID=8YFLogxK

U2 - 10.1016/j.schres.2007.01.019

DO - 10.1016/j.schres.2007.01.019

M3 - Article

C2 - 17363222

AN - SCOPUS:34147102249

VL - 92

SP - 108

EP - 115

JO - Schizophrenia Research

JF - Schizophrenia Research

SN - 0920-9964

IS - 1-3

ER -