IL-1β knock-down in the hippocampus alleviates lipopolysaccharide-induced memory deficits, depression-and anxiety-like behavior in mice
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- 英文论文题名：IL-1β knock-down in the hippocampus alleviates lipopolysaccharide-induced memory deficits, depression-and anxiety-like behavior in mice
- 论文作者：Chenli Li ; Mengmeng Li ; Jiacheng Geng ; Xiongxiong Cai ; Hanjie Yu ; 王闯 ; Qingwen Wang
- 英文论文作者：Chenli Li ; Mengmeng Li ; Jiacheng Geng ; Xiongxiong Cai ; Hanjie Yu ; Chuang Wang ; Qingwen Wang ; Ningbo Key Laboratory of Behavioral Neuroscience ; Zhejiang Provincial Key Laboratory of Pathophysiology ; School of Medicine ; Ningbo University
- 年：2016
- 作者机构：Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University;
- 会议召开时间：2016-09-24
- 会议录名称：长三角地区神经科学论坛2016暨第八次会员代表大会摘要集
- 语种：英文
- 分类号：R749
- 学会代码：ZGSK
- 会议名称：长三角地区神经科学论坛2016暨第八次会员代表大会
- 会议地点：中国上海
- 主办单位：上海市神经科学学会
- 学会名称：中国神经科学学会
- 页数：2
- 文件大小：528k
- 原文格式：D
- 会议级别：地方
摘要
Peripheral inflammatory responses affect central nervous system(CNS) function, the main symptoms involve memory deficits, depression and anxiety. Interleukin-1β(IL-1β), a proinflammatory cytokine, has been proposed to be a key mediator in a variety of behavioral actions of stress. The objective of this study was to explore the involvement of Nrf2 and biochemical alterations of inflammatory or oxidative stress markers in the alleviating effects of IL-1β knock-down on lipopolysaccharide-induced memory deficits, depression-and anxiety-like behavior in mice. The mice were treated with either IL-1β-RNAi lentivirus(1μg/side) or vehicle lentivirus(1μg/side) by microinjection into CA1 subregions of hippocampus. After 7 days recovery, LPS(1 mg/kg, i.p.) or saline were administrated. The behavioral tests for memory deficits were conducted on novel object recognition test(NORT), and for the depression-like behaviors were performed by sucrose preference test(SPT) and forced swim test(FST) and for the anxiety-like behaviors were examined by zero maze in mice. Furthermore, expressions of Nrf2 were examined by western blotting, and the inflammatory factors(IL-1β and TNF-α) and the brain-derived neurotrophic factor(BDNF) were assayed by ELISA kit. The oxidative stress markers of malonaldehyde(MDA), SOD and nitric oxide(NO) were performed by commercial colorimetric kit assays. Our results demonstrated that IL-1β knock-down significantly attenuated LPS-induced memory deficits, depression-like and anxiety-like behaviors in mice. In addition, IL-1β knock-down ameliorated LPS-induced neuroinflammation responses by reducing IL-1β and TNF-α levels in hippocampus. Further, IL-1β knock-down also prevented LPS evoked oxidative stress via restored brain pro-oxidant/anti-oxidant balance by inhibiting MDA, SOD and NO concentrations. Finally, we also confirmed that IL-1β knock-down reversed the downregulation of Nrf2 induced by LPS. In conclusion, our results may suggest that co-morbid depression, anxiety and memory deficits associated with inflammatory and oxidative stress responses. Our results also strongly speculated that the IL-1β control could be a therapeutic approach for the treatment of co-morbid disorders which are closely associated with neuroinflammation and oxidative stress.
Peripheral inflammatory responses affect central nervous system(CNS) function, the main symptoms involve memory deficits, depression and anxiety. Interleukin-1β(IL-1β), a proinflammatory cytokine, has been proposed to be a key mediator in a variety of behavioral actions of stress. The objective of this study was to explore the involvement of Nrf2 and biochemical alterations of inflammatory or oxidative stress markers in the alleviating effects of IL-1β knock-down on lipopolysaccharide-induced memory deficits, depression-and anxiety-like behavior in mice. The mice were treated with either IL-1β-RNAi lentivirus(1μg/side) or vehicle lentivirus(1μg/side) by microinjection into CA1 subregions of hippocampus. After 7 days recovery, LPS(1 mg/kg, i.p.) or saline were administrated. The behavioral tests for memory deficits were conducted on novel object recognition test(NORT), and for the depression-like behaviors were performed by sucrose preference test(SPT) and forced swim test(FST) and for the anxiety-like behaviors were examined by zero maze in mice. Furthermore, expressions of Nrf2 were examined by western blotting, and the inflammatory factors(IL-1β and TNF-α) and the brain-derived neurotrophic factor(BDNF) were assayed by ELISA kit. The oxidative stress markers of malonaldehyde(MDA), SOD and nitric oxide(NO) were performed by commercial colorimetric kit assays. Our results demonstrated that IL-1β knock-down significantly attenuated LPS-induced memory deficits, depression-like and anxiety-like behaviors in mice. In addition, IL-1β knock-down ameliorated LPS-induced neuroinflammation responses by reducing IL-1β and TNF-α levels in hippocampus. Further, IL-1β knock-down also prevented LPS evoked oxidative stress via restored brain pro-oxidant/anti-oxidant balance by inhibiting MDA, SOD and NO concentrations. Finally, we also confirmed that IL-1β knock-down reversed the downregulation of Nrf2 induced by LPS. In conclusion, our results may suggest that co-morbid depression, anxiety and memory deficits associated with inflammatory and oxidative stress responses. Our results also strongly speculated that the IL-1β control could be a therapeutic approach for the treatment of co-morbid disorders which are closely associated with neuroinflammation and oxidative stress.
Peripheral inflammatory responses affect central nervous system(CNS) function, the main symptoms involve memory deficits, depression and anxiety. Interleukin-1β(IL-1β), a proinflammatory cytokine, has been proposed to be a key mediator in a variety of behavioral actions of stress. The objective of this study was to explore the involvement of Nrf2 and biochemical alterations of inflammatory or oxidative stress markers in the alleviating effects of IL-1β knock-down on lipopolysaccharide-induced memory deficits, depression-and anxiety-like behavior in mice. The mice were treated with either IL-1β-RNAi lentivirus(1μg/side) or vehicle lentivirus(1μg/side) by microinjection into CA1 subregions of hippocampus. After 7 days recovery, LPS(1 mg/kg, i.p.) or saline were administrated. The behavioral tests for memory deficits were conducted on novel object recognition test(NORT), and for the depression-like behaviors were performed by sucrose preference test(SPT) and forced swim test(FST) and for the anxiety-like behaviors were examined by zero maze in mice. Furthermore, expressions of Nrf2 were examined by western blotting, and the inflammatory factors(IL-1β and TNF-α) and the brain-derived neurotrophic factor(BDNF) were assayed by ELISA kit. The oxidative stress markers of malonaldehyde(MDA), SOD and nitric oxide(NO) were performed by commercial colorimetric kit assays. Our results demonstrated that IL-1β knock-down significantly attenuated LPS-induced memory deficits, depression-like and anxiety-like behaviors in mice. In addition, IL-1β knock-down ameliorated LPS-induced neuroinflammation responses by reducing IL-1β and TNF-α levels in hippocampus. Further, IL-1β knock-down also prevented LPS evoked oxidative stress via restored brain pro-oxidant/anti-oxidant balance by inhibiting MDA, SOD and NO concentrations. Finally, we also confirmed that IL-1β knock-down reversed the downregulation of Nrf2 induced by LPS. In conclusion, our results may suggest that co-morbid depression, anxiety and memory deficits associated with inflammatory and oxidative stress responses. Our results also strongly speculated that the IL-1β control could be a therapeutic approach for the treatment of co-morbid disorders which are closely associated with neuroinflammation and oxidative stress.
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