CNS neuroscience & therapeutics · 2013
Involvement of inflammasome activation in lipopolysaccharide-induced mice depressive-like behaviors.
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Zhang Yi, Liu Lei, Peng Yun-Li, Liu Yun-Zi, Wu Teng-Yun, Shen Xiao-Liang, Zhou Jiang-Rui, Sun Ding-Ya, Huang Ai-Jun, Wang Xia, Wang Yun-Xia, Jiang Chun-Lei
Аннотация
AIMS: The NLRP3 inflammasome is a cytoplasmic multiprotein complex of the innate immune system that regulates the cleavage of interleukin-1β and interleukin-18 precursors. It can detect a wide range of danger signals and trigger a series of immune-inflammatory reactions. There were plenty of studies indicating that activation of the immune system played pivotal roles in depression. However, the underlying mechanisms of immune-depression interactions remained elusive and there was no report about the involvement of inflammasome activation in depression.
METHODS: We established an acute depression mouse model with lipopolysaccharide to explore the involvement of inflammasome activation in depression.
RESULTS: The lipopolysaccharide-treated mice displayed depressive-like behaviors and pro-inflammatory cytokine interleukin-1β protein and mRNA levels significantly increased. The NLRP3 inflammasome mRNA expression level also significantly elevated in depressed mice brain. Pretreatment with the NLRP3 inflammasome inhibitor Ac-YVAD-CMK significantly abrogated the depressive-like behaviors induced by lipopolysaccharide.
CONCLUSION: These data suggest for the first time that the NLRP3 inflammasome is involved in lipopolysaccharide-induced mice depressive-like behaviors. The NLRP3 inflammasome may be a central mediator between immune activation and depression, which raises the possibility that it may be a more specific target for the depression treatments in the near future.
METHODS: We established an acute depression mouse model with lipopolysaccharide to explore the involvement of inflammasome activation in depression.
RESULTS: The lipopolysaccharide-treated mice displayed depressive-like behaviors and pro-inflammatory cytokine interleukin-1β protein and mRNA levels significantly increased. The NLRP3 inflammasome mRNA expression level also significantly elevated in depressed mice brain. Pretreatment with the NLRP3 inflammasome inhibitor Ac-YVAD-CMK significantly abrogated the depressive-like behaviors induced by lipopolysaccharide.
CONCLUSION: These data suggest for the first time that the NLRP3 inflammasome is involved in lipopolysaccharide-induced mice depressive-like behaviors. The NLRP3 inflammasome may be a central mediator between immune activation and depression, which raises the possibility that it may be a more specific target for the depression treatments in the near future.
Предметные рубрики MeSH
Amino Acid Chloromethyl KetonesAnimalsBrainCarrier ProteinsCaspase 1Cysteine Proteinase InhibitorsDepressionDisease Models, AnimalDrug Administration ScheduleFood PreferencesGene Expression RegulationInflammationInterleukin-1betaLipopolysaccharidesMaleMiceMice, Inbred BALB CNLR Family, Pyrin Domain-Containing 3 ProteinRNA, MessengerSucroseSwimming