Abstract:
:Systemic inflammation often induces neuroinflammation and disrupts neural functions, ultimately causing cognitive impairment. Furthermore, neuronal inflammation is the key cause of many neurological conditions. It is particularly important to develop effective neuroprotectants to prevent and control inflammatory brain diseases. Baicalin (BAI) has a wide variety of potent neuroprotective and cognitive enhancement properties in various models of neuronal injury through antioxidation, anti-inflammation, anti-apoptosis, and stimulating neurogenesis. Nevertheless, it remains unclear whether BAI can resolve neuroinflammation and cognitive decline triggered by systemic or distant inflammatory processes. In the present study, intraperitoneal lipopolysaccharide (LPS) administration was used to establish neuroinflammation to evaluate the potential neuroprotective and anti-inflammatory effects of BAI. Here, we report that BAI activated silent information regulator 1 (SIRT1) to deacetylate high-mobility group box 1 (HMGB1) protein in response to acute LPS-induced neuroinflammation and cognitive deficits. Furthermore, we demonstrated the anti-inflammatory and cognitive enhancement effects and the underlying molecular mechanisms of BAI in modulating microglial activation and systemic cytokine production, including tumor necrosis factor- (TNF-) α and interleukin- (IL-) 1β, after LPS exposure in mice and in the microglial cell line, BV2. In the hippocampus, BAI not only reduced reactive microglia and inflammatory cytokine production but also modulated SIRT1/HMGB1 signaling in microglia. Interestingly, pretreatment with SIRT1 inhibitor EX-527 abolished the beneficial effects of BAI against LPS exposure. Specifically, BAI treatment inhibited HMGB1 release via the SIRT1/HMGB1 pathway and reduced the nuclear translocation of HMGB1 in LPS-induced BV2 cells. These effects were reversed in BV2 cells by silencing endogenous SIRT1. Taken together, these findings indicated that BAI reduced microglia-associated neuroinflammation and improved acute neurocognitive deficits in LPS-induced mice via SIRT1-dependent downregulation of HMGB1, suggesting a possible novel protection against acute neurobehavioral deficits, such as delayed neurocognitive recovery after anesthesia and surgery challenges.
journal_name
Oxid Med Cell Longevjournal_title
Oxidative medicine and cellular longevityauthors
Li Y,Liu T,Li Y,Han D,Hong J,Yang N,He J,Peng R,Mi X,Kuang C,Zhou Y,Han Y,Shi C,Li Z,Guo Xdoi
10.1155/2020/4751349subject
Has Abstractpub_date
2020-09-22 00:00:00pages
4751349eissn
1942-0900issn
1942-0994journal_volume
2020pub_type
杂志文章abstract::This work reviews concepts regarding oxidative stress and the mechanisms by which endogenous and exogenous factors produce reactive oxygen species (ROS). It also surveys the relationships between oxidative stress, circadian rhythms, and retinal damage in humans, particularly those related to light and photodamage. In ...
journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章,评审
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journal_title:Oxidative medicine and cellular longevity
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journal_title:Oxidative medicine and cellular longevity
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pub_type: 杂志文章
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更新日期:2015-01-01 00:00:00
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pub_type: 杂志文章,评审
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章,评审
doi:10.1155/2016/3578368
更新日期:2016-01-01 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2018/8753063
更新日期:2018-03-21 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章,评审
doi:10.1155/2016/1067801
更新日期:2016-01-01 00:00:00
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journal_title:Oxidative medicine and cellular longevity
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doi:10.1155/2020/3076131
更新日期:2020-02-27 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2017/6934394
更新日期:2017-01-01 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章,评审
doi:10.1155/2016/6021934
更新日期:2016-01-01 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2016/6981595
更新日期:2016-01-01 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2019/9246138
更新日期:2019-10-09 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2018/3812568
更新日期:2018-01-21 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章,评审
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更新日期:2016-01-01 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2020/7627934
更新日期:2020-11-23 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2019/1821969
更新日期:2019-04-16 00:00:00
abstract::Oxidative stress is crucially involved in the pathogenesis of neurological diseases such as stroke and degenerative diseases. We previously demonstrated that platelet-derived growth factors (PDGFs) protected neurons from H2O2-induced oxidative stress and indicated the involvement of PI3K-Akt and MAP kinases as an unde...
journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
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更新日期:2013-01-01 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2018/4596746
更新日期:2018-07-29 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
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更新日期:2020-01-20 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2019/6051262
更新日期:2019-04-08 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章,评审
doi:10.1155/2019/7210892
更新日期:2019-06-16 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
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更新日期:2018-12-23 00:00:00
abstract::[This corrects the article DOI: 10.1155/2018/7861518.]. ...
journal_title:Oxidative medicine and cellular longevity
pub_type: 已发布勘误
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章,评审
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更新日期:2019-05-12 00:00:00