CXCL8 gene silencing promotes neuroglial cells activation while inhibiting neuroinflammation through the PI3K/Akt/NF‐κB‐signaling pathway in mice with ischemic stroke

Lv, Hui; Li, Jie; Che, Yuqin

doi:10.1002/jcp.27493

Cited by 41 publications

(27 citation statements)

References 47 publications

(72 reference statements)

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“…In a mouse IS model, the expression of IL-8 in peripheral mononuclear cells could affect the occurrence of IS by regulating the PI3K/Akt/NF-kb signaling pathway. After reducing the expression of IL-8, it reduced the infarct size, activated the neurogliocytes, and improved neural function recovery (Lv et al, 2019). This study further suggests that IL-8 expression in the brain increases in patients with DM, as do the activities of the NF-κB, MAPK, TNF, and PI3K-Akt signaling pathways.…”

Section: Discussionsupporting

confidence: 52%

RNA-seq analysis of ischemia stroke and normal brain in a tree shrew model with or without type 2 diabetes mellitus

et al. 2021

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Background: Nowadays, similar strategies have been used for the treatment and prevention of acute stroke in both diabetes mellitus (DM) and non-DM populations. These strategies were analyzed to provide an experimental basis for the clinical prevention and treatment of stroke in patients both with and without DM. Methods: Tree shrews were randomly divided into control, DM, ischemic stroke (IS), and DMIS groups with 18 animals in each group. Serum biochemical indicators were used to assess metabolic status. Neural tissue damage was determined using triphenyl tetrazolium chloride staining, H-E staining, and electron microscopy. Differential gene expression of neural tissue between the DM and control groups and the IS and DMIS groups was measured using RNA-seq analysis.Results: The serum glucose levels of the DM and DMIS groups were signi cantly higher than other groups.In the DMIS group, the infarct size was signi cantly larger than in the IS group (19.56 ± 1.25%), with a more obvious abnormal ultrastructure of neural cells. RNA-seq analysis showed that the expression of IL-8, C-C motif chemokine 2 (CCL2), and alpha-1-antichymotrypsin was signi cantly higher in the DM group than in the control group. The CCL7, ATP-binding cassette sub-family A member 12, and adhesion G protein-coupled receptor E2 levels were signi cantly higher in the DMIS group than in the IS group.Conclusions: For the prevention and treatment of stroke in patients with DM, reducing the in ammatory state of the nervous system may reduce the incidence of stroke and improve the prognosis of neurological function after IS.

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Section: Discussionsupporting

confidence: 52%

RNA-seq analysis of ischemia stroke and normal brain in a tree shrew model with or without type 2 diabetes mellitus

et al. 2021

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“…Research studies have confirmed that activation of NFthe ‐κB signal pathway widely exists in various kinds of CNS damages, including ischemic stroke, 63 , 64 , 65 ICH, 44 , 45 , 66 and SAH, 36 , 67 and its repression could notably reduce these brain impairments. 36 , 63 , 64 , 65 , 67 In our previous research, we also have verified that NF‐κB signal pathway‐related proteins were significantly upregulated after ICH, and its suppression could markedly alleviate ICH‐induced EBI and neurobehavioral deficiency. 44 , 45 Similarly, our current results suggest that PUE could significantly improve ICH‐induced EBI and related molecular mechanisms possibly by PI3K/Akt signal activation‐mediated suppression of the NF‐κB pathway.…”

Section: Discussionmentioning

confidence: 96%

Puerarin attenuates intracerebral hemorrhage‐induced early brain injury possibly by PI3K/Akt signal activation‐mediated suppression of NF‐κB pathway

Zeng

Zheng

Chen

et al. 2021

J Cellular Molecular Medi

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Intracerebral hemorrhage (ICH) can induce intensively oxidative stress, neuroinflammation, and brain cell apoptosis. However, currently, there is no highly effective treatment available. Puerarin (PUE) possesses excellent neuroprotective effects by suppressing the NF‐κB pathway and activating the PI3K/Akt signal, but its role and related mechanisms in ICH‐induced early brain injury (EBI) remain unclear. In this study, we intended to observe the effects of PUE and molecular mechanisms on ICH‐induced EBI. ICH was induced in rats by collagenase IV injection. PUE was intraperitoneally administrated alone or with simultaneously intracerebroventricular injection of LY294002 (a specific inhibitor of the PI3K/Akt signal). Neurological deficiency, histological impairment, brain edema, hematoma volume, blood–brain barrier destruction, and brain cell apoptosis were evaluated. Western blot, immunohistochemistry staining, reactive oxygen species (ROS) measurement, and enzyme‐linked immunosorbent assay were performed. PUE administration at 50 mg/kg and 100 mg/kg could significantly reduce ICH‐induced neurological deficits and EBI. Moreover, PUE could notably restrain ICH‐induced upregulation of the NF‐κB pathway, pro‐inflammatory cytokines, ROS level, and apoptotic pathway and activate the PI3K/Akt signal. However, LY294002 delivery could efficaciously weaken these neuroprotective effects of PUE. Overall, PUE could attenuate ICH‐induced behavioral defects and EBI possibly by PI3K/Akt signal stimulation‐mediated inhibition of the NF‐κB pathway, and this made PUE a potential candidate as a promising therapeutic option for ICH‐induced EBI.

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“…The sections were examined and photographed under fluorescence microscopy (DFC310 FX, Leica, Germany). Apoptosis index (AI) = apoptotic cell number/total cell number × 100% [17].…”

Section: Methodsmentioning

confidence: 99%

Jiawei Foshou San Induces Apoptosis in Ectopic Endometrium Based on Systems Pharmacology, Molecular Docking, and Experimental Evidence

Jiang

Zhao

Zhang

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Foshou San is a typical gynaecological formula with wild usage in traditional Chinese medicine. Jiawei Foshou San (JFS) is a novel ingredient prescription from Foshou San with antiendometriosis effect in unclear mechanisms. To uncover the potential application and proapoptotic mechanisms of JFS, JFS ingredient-drug target-disease networks, GO enrichment, and pathway analysis were established for potential application prediction. Molecular docking and validation in vivo were investigated by the proapoptotic mechanisms of JFS. In this study, 99 common targets were related to 108 diseases. 484 biological processes, 44 cell components, 59 molecular functions, and 37 pathways were significantly identified in GO enrichment and pathway analysis. In molecular docking, ligustrazine showed binding activity with Bcl-2, Bax, caspase-9, caspase-3, and PARP. In vivo, JFS elevated the shrink rate of ectopic endometrium, by suppressing E2 and PROG. An in-depth study showed that apoptosis was activated through diminishing Bcl-2, rising Bax and Bad, and expressing more caspase-3 and caspase-9 using JFS. JFS promoted the protein level of cleaved-PARP. In brief, JFS might be applied for various diseases through multiple targets and pathways, especially endometriosis by Bcl-2 pathway. These findings reveal the potential application for further evaluation and uncover the proapoptotic mechanism of JFS.

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CXCL8 gene silencing promotes neuroglial cells activation while inhibiting neuroinflammation through the PI3K/Akt/NF‐κB‐signaling pathway in mice with ischemic stroke

Cited by 41 publications

References 47 publications

RNA-seq analysis of ischemia stroke and normal brain in a tree shrew model with or without type 2 diabetes mellitus

RNA-seq analysis of ischemia stroke and normal brain in a tree shrew model with or without type 2 diabetes mellitus

Puerarin attenuates intracerebral hemorrhage‐induced early brain injury possibly by PI3K/Akt signal activation‐mediated suppression of NF‐κB pathway

Jiawei Foshou San Induces Apoptosis in Ectopic Endometrium Based on Systems Pharmacology, Molecular Docking, and Experimental Evidence

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