Abstract:
:Oxidative stress (OS) and neuronal apoptosis are major pathological processes after hypoxic-ischemic encephalopathy (HIE). Colony stimulating factor 1 (CSF1), binding to CSF1 receptor (CSF1R), has been shown to reduce neuronal loss after hypoxic-ischemia- (HI-) induced brain injury. In the present study, we hypothesized that CSF1 could alleviate OS-induced neuronal degeneration and apoptosis through the CSF1R/PLCG2/PKA/UCP2 signaling pathway in a rat model of HI. A total of 127 ten-day old Sprague Dawley rat pups were used. HI was induced by right common carotid artery ligation with subsequent exposure to hypoxia for 2.5 h. Exogenous recombinant human CSF1 (rh-CSF1) was administered intranasally at 1 h and 24 h after HI. The CSF1R inhibitor, BLZ945, or phospholipase C-gamma 2 (PLCG2) inhibitor, U73122, was injected intraperitoneally at 1 h before HI induction. Brain infarct volume measurement, cliff avoidance test, righting reflex test, double immunofluorescence staining, western blot assessment, 8-OHdG and MitoSOX staining, Fluoro-Jade C staining, and TUNEL staining were used. Our results indicated that the expressions of endogenous CSF1, CSF1R, p-CSF1R, p-PLCG2, p-PKA, and uncoupling protein2 (UCP2) were increased after HI. CSF1 and CSF1R were expressed in neurons and astrocytes. Rh-CSF1 treatment significantly attenuated neurological deficits, infarct volume, OS, neuronal apoptosis, and degeneration at 48 h after HI. Moreover, activation of CSF1R by rh-CSF1 significantly increased the brain tissue expressions of p-PLCG2, p-PKA, UCP2, and Bcl2/Bax ratio, but reduced the expression of cleaved caspase-3. The neuroprotective effects of rh-CSF1 were abolished by BLZ945 or U73122. These results suggested that rh-CSF1 treatment attenuated OS-induced neuronal degeneration and apoptosis after HI, at least in part, through the CSF1R/PLCG2/PKA/UCP2 signaling pathway. Rh-CSF1 may serve as therapeutic strategy against brain damage in patients with HIE.
journal_name
Oxid Med Cell Longevjournal_title
Oxidative medicine and cellular longevityauthors
Hu X,Li S,Doycheva DM,Huang L,Lenahan C,Liu R,Huang J,Gao L,Tang J,Zuo G,Zhang JHdoi
10.1155/2020/6801587subject
Has Abstractpub_date
2020-10-07 00:00:00pages
6801587eissn
1942-0900issn
1942-0994journal_volume
2020pub_type
杂志文章abstract::Programmed and damage aging theories have traditionally been conceived as stand-alone schools of thought. However, the p66Shc adaptor protein has demonstrated that aging-regulating genes and reactive oxygen species (ROS) are closely interconnected, since its absence modifies metabolic homeostasis by providing oxidativ...
journal_title:Oxidative medicine and cellular longevity
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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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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
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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
pub_type: 杂志文章
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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
pub_type: 杂志文章
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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
pub_type: 已发布勘误
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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
doi:10.1155/2020/5281795
更新日期:2020-12-08 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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journal_title:Oxidative medicine and cellular longevity
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2019/3492767
更新日期:2019-08-14 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2014/329172
更新日期:2014-01-01 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:2020-04-22 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2013/612784
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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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doi:10.4161/oxim.2.2.8361
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章,评审
doi:10.1155/2012/740849
更新日期:2012-01-01 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2015/124357
更新日期:2015-01-01 00:00:00
abstract::Fructose corn syrup is cheap sweetener and prolongs the shelf life of products, but fructose intake causes hyperinsulinemia, hypertriglyceridemia, and hypertension. All of them are referred to as metabolic syndrome and they are risk factors for cardiovascular diseases. Hence, the harmful effects of increased fructose ...
journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2016/3419479
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:10.1155/2014/735618
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2020/6340190
更新日期:2020-06-16 00:00:00
abstract::Transient receptor potential vanilloid 1 (TRPV1) is a Ca+2-permeable channel expressed on neuronal and nonneuronal cells, known as an oxidative stress sensor. It plays a protective role in bacterial infection, and recent findings indicate that this receptor modulates monocyte populations in mice with malaria; however,...
journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2019/9451671
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2018/4528581
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abstract:BACKGROUND AND AIMS:Metabolic syndrome (MetS) has been associated with occurrence and prognosis of ischemic stroke. This study aimed to evaluate whether an association exists between MetS and early neurological deterioration (END) following acute ischemic stroke and the possible role inflammatory biomarkers play. METH...
journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2016/8346301
更新日期:2016-01-01 00:00:00
abstract::Background. Oxidative stress plays an important role in the pathogenesis of contrast-induced nephropathy (CIN). The aim of this study was to investigate the antioxidant effects of sulforaphane (SFN) in a rat model of CIN and a cell model of oxidative stress in HK2 cells. Methods. Rats were randomized into four groups ...
journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2016/9825623
更新日期:2016-01-01 00:00:00