TY - JOUR
T1 - Protective effects of nicergoline against neuronal cell death induced by activated microglia and astrocytes
AU - Mizuno, Tetsuya
AU - Kuno, Reiko
AU - Nitta, Atsumi
AU - Nabeshima, Toshitaka
AU - Zhang, Guiqin
AU - Kawanokuchi, Jun
AU - Wang, Jinyan
AU - Jin, Shijie
AU - Takeuchi, Hideyuki
AU - Suzumura, Akio
N1 - Funding Information:
This work was supported in part by a Grant-in-aid for Scientific Research (Grant C), the Creation of Innovations through Business–Academic–Public Sector Cooperation, and the 21st Century COE program “Integrated Molecular Medicine for Neuronal and Neoplastic Disorders” from the Japanese Ministry of Education, Science, and Culture, and for the Research on Specific Diseases from the Japanese Ministry of Health, Labour, and Welfare.
PY - 2005/12/20
Y1 - 2005/12/20
N2 - We examined the neuroprotective role of nicergoline in neuron-microglia or neuron-astrocytes co-cultures. Nicergoline, an ergoline derivative, significantly suppressed the neuronal cell death induced by co-culture with activated microglia or astrocytes stimulated with lipopolysaccharide (LPS) and interferon (IFN)-γ. To elucidate the mechanism by which nicergoline exerts a neuroprotective effect, we examined the production of inflammatory mediators and neurotrophic factors in activated microglia and astrocytes following nicergoline treatment. In microglia stimulated with LPS and IFN-γ, nicergoline suppressed the production of superoxide anions, interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in a dose-dependent manner. In astrocytes, nicergoline also suppressed the production of proinflammatory cytokines and enhanced brain-derived neurotrophic factor (BDNF). Thus, nicergoline-mediated neuroprotection resulted primarily from the inhibition of inflammatory mediators and the upregulation of neurotrophic factors by glial cells.
AB - We examined the neuroprotective role of nicergoline in neuron-microglia or neuron-astrocytes co-cultures. Nicergoline, an ergoline derivative, significantly suppressed the neuronal cell death induced by co-culture with activated microglia or astrocytes stimulated with lipopolysaccharide (LPS) and interferon (IFN)-γ. To elucidate the mechanism by which nicergoline exerts a neuroprotective effect, we examined the production of inflammatory mediators and neurotrophic factors in activated microglia and astrocytes following nicergoline treatment. In microglia stimulated with LPS and IFN-γ, nicergoline suppressed the production of superoxide anions, interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in a dose-dependent manner. In astrocytes, nicergoline also suppressed the production of proinflammatory cytokines and enhanced brain-derived neurotrophic factor (BDNF). Thus, nicergoline-mediated neuroprotection resulted primarily from the inhibition of inflammatory mediators and the upregulation of neurotrophic factors by glial cells.
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U2 - 10.1016/j.brainres.2005.10.050
DO - 10.1016/j.brainres.2005.10.050
M3 - Article
C2 - 16325157
AN - SCOPUS:29044446068
VL - 1066
SP - 78
EP - 85
JO - Molecular Brain Research
JF - Molecular Brain Research
SN - 0006-8993
IS - 1-2
ER -