Cerebral ischemia-reperfusion aggravated cerebral infarction injury and possible differential genes identified by RNA-Seq in rats

Xiao, Cheng; Yang, Yinglin; Li, Wei-Han; Liu, Man; Wang, Yuehua; Du, Guanhua

doi:10.1016/j.brainresbull.2019.12.014

Cited by 23 publications

(9 citation statements)

References 35 publications

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“… 28 In addition, cerebral I/R-induced the upregulation of genes belonged to the TLR4/MyD88/NF-кB signaling and then aggravated cerebral infarction damage, revealing that the TLR4/MyD88/NF-кB signaling may be a promising therapeutic approach for ischemic stroke. 29 Interestingly, there is evidence to suggest that TNIP1 expression was downregulated in hepatic I/R mice and its upregulation could alleviate hepatic I/R-induced inflammatory response and apoptosis via the TLR4/MyD88/NF-кB signaling. 30 Nevertheless, whether the TLR4/MyD88/NF-кB signaling is involved in the TNIP2-mediated neuroprotective effect still needs to be determined.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Function of TNFAIP3 Interacting Protein 2 Against Oxygen and Glucose Deprivation/Reoxygenation-Induced Injury in Hippocampal Neuronal HT22 Cells Through Regulation of the TLR4/MyD88/NF-κB Pathway

Yan¹,

Chen²,

Zhang³

et al. 2021

NDT

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Background: Tumor necrosis factor-α (TNF-α)-induced protein 3-interacting protein 2 (TNIP2) has been well demonstrated to act as a principal contributor to the development of inflammatory diseases; however, the role of TNIP2 in cerebral ischemic/reperfusion injury has never been studied. Methods: Gene expression was examined by using quantitative real-time polymerase chain reaction and Western blot. The functional role of TNIP2 in oxygen and glucose deprivation/ reoxygenation (OGD/R)-induced neuronal injury was evaluated using cell counting kit-8, terminal deoxynucleotidyl transferase dutp nick end labeling assay and enzyme-linked immunosorbent assay. Commercial kits were applied to evaluate the activity of NF-kappa -B (NF-κB) and caspase-3, as well as the release of lactate dehydrogenase release (LDH). Results: TNIP2 expression was substantially declined in HT22 cells following OGD/R stimulation. TNIP2 overexpression attenuated ODG/R-induced inflammation in HT22 cells, as evidenced by reduced levels of TNF-α, interleukin (IL)-1β, and intercellular cell adhesion molecule-1 (ICAM-1), and increased levels of IL-10. TNIP2 overexpression also reduced activity of NF-κB under ODG/R condition. Meanwhile, OGD/R treatment caused a reduction of cell viability and an elevation of cell apoptosis in HT22 cells, as indicated by the increase in LDH and caspase-3 activity. Whereas, OGD/R-induced HT22 cell injury was mitigated by TNIP2 overexpression in HT22 cells. Besides, we found the involvement of toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/NF-κB pathway in the neuroprotective effect of TNIP2 on OGD/R-induced HT22 cell damage. Conclusion: TNIP2 overexpression mitigates OGD/R-induced inflammatory response and apoptosis. Moreover, TLR4/MyD88/NF-κB pathway participates in the protective effect of TNIP2 on OGD/R-induced neuronal damage.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective Function of TNFAIP3 Interacting Protein 2 Against Oxygen and Glucose Deprivation/Reoxygenation-Induced Injury in Hippocampal Neuronal HT22 Cells Through Regulation of the TLR4/MyD88/NF-κB Pathway

Yan¹,

Chen²,

Zhang³

et al. 2021

NDT

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“…The brains were removed and prefixed in 4% PFA for 48 h and dehydrated in gradient ethanol, transparentized by xylene, embedded in paraffin, and cut coronally in the SVZ into pieces of 5-μm thickness, then adhered to the glass slices. Then immunofluorescence was performed as described previously [ 18 ]. Anti-Nestin antibody produced in rabbit (1: 100, Boster, Wuhan, China), anti-β-Tubulin III antibody produced in rabbit (1: 70, Sigma, Missouri, USA), anti-O4 antibody produced in mouse (1: 50, Sigma, Missouri, USA), and anti-GFAP antibody produced in mouse (1: 500, CST, Danvers, USA) were used as primary antibodies, and FITC- (1: 50) and Cy3- (1: 70) were used as secondary antibodies (Boster, Wuhan, China).…”

Section: Methodsmentioning

confidence: 99%

Astragalus Flavone Induces Proliferation and Differentiation of Neural Stem Cells in a Cerebral Infarction Model

et al. 2021

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Background Ischemic cerebrovascular disease leads to the activation and differentiation of neural stem cells (NSCs) into mature neurons and glia cells to repair nerve damage. Astragalus flavone (ASF) has shown its potential role in proliferation and differentiation into dopamine neurons of NSCs. Material/Methods Cerebral infarction models were constructed to determine the effects of ASF on NSCs in vivo and in vitro. Results ASF therapy had the ability to reduce the neurologic function scores and the cerebral infarction volume of the cerebral infarction model. Moreover, ASF was able to increase BrdU-positive cells and promote the expression of Nestin, β-Tubulin III, and O4, while decreasing the expression of GFAP. qRT-PCR and western blot assays showed ASF promoted the expression of Mash1, Math1, and Ngn2 mRNA and protein in cerebral infarction rats. Meanwhile, ASF (20 μg/ml) was able to increase EdU-positive cells and promote the expression of Nestin, β-Tubulin III, and O4 of NSCs at day14 in vitro. In normoxia, ASF obviously promoted the expression of Mash1, Ngn1, and Ngn2 mRNA and proteins, but in hypoxia, ASF promoted the expression of Notch1 and Math1 mRNA and proteins and inhibited the expression of Ngn1 and Ngn2 mRNA and proteins. Conclusions ASF therapy can improve the neurologic functions and reduce the cerebral infarction volume in a cerebral infarction model. Moreover, ASF promoted the proliferation of NSCs and induced differentiation into neurons and oligodendrocytes, which might be involved in regulating factors in Notch signaling.

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“…The raw sequences were processed for quality control, trimming (Trimmomatic version 0.36) [ 44 ], and alignment (STAR/2.5.1b). Downstream analyses were performed by using R (version3.1.1, RStudio, Boston, MA, USA), with edgeR and limma package with voom method [ 45 ]. After the statistical analysis, p-values with the means of the two groups were calculated.…”

Section: Methodsmentioning

confidence: 99%

RKC-B1 Blocks Activation of NF-κB and NLRP3 Signaling Pathways to Suppress Neuroinflammation in LPS-Stimulated Mice

et al. 2021

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RKC-B1 is a novel fermentation product obtained from the marine micromonospora FIM02-523A. Thus far, there have been few reports about the pharmacological activity of RKC-B1. In our present study, we investigated the anti-neuroinflammatory effects and the possible mechanism of RKC-B1 in LPS-stimulated mice. After treatment with RKC-B1, RNA-seq transcriptome of the cerebral cortex tissue was conducted to find the differentially expressed genes (DEGs). Inflammatory cytokines and proteins were evaluated by ELISA and WB. In RNA-seq analysis, there were 193 genes screened as core genes of RKC-B1 for treatment with neuroinflammation. The significant KEGG enrichment signaling pathways of these core genes were mainly included TNF signaling pathway, IL-17 signaling pathway, NOD-like receptor signaling pathway, NF-κB signaling pathway and others. The corresponding top five KEGG enrichment pathways of three main clusters in PPI network of core genes were closely related to human immune system and immune disease. The results showed that RKC-B1 reduced the levels of pro-inflammatory factors (IL-6, IL-1β, MCP-1, and ICAM-1) and the expression of COX2 in cerebral cortex tissue. Additionally, we found that the anti-neuroinflammation activity of RKC-B1 might be related to suppress activating of NF-κB and NLRP3/cleaved caspase-1 signaling pathways. The current findings suggested that RKC-B1 might be a promising anti-neuroinflammatory agent.

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Cerebral ischemia-reperfusion aggravated cerebral infarction injury and possible differential genes identified by RNA-Seq in rats

Cited by 23 publications

References 35 publications

Neuroprotective Function of TNFAIP3 Interacting Protein 2 Against Oxygen and Glucose Deprivation/Reoxygenation-Induced Injury in Hippocampal Neuronal HT22 Cells Through Regulation of the TLR4/MyD88/NF-κB Pathway

Neuroprotective Function of TNFAIP3 Interacting Protein 2 Against Oxygen and Glucose Deprivation/Reoxygenation-Induced Injury in Hippocampal Neuronal HT22 Cells Through Regulation of the TLR4/MyD88/NF-κB Pathway

Astragalus Flavone Induces Proliferation and Differentiation of Neural Stem Cells in a Cerebral Infarction Model

RKC-B1 Blocks Activation of NF-κB and NLRP3 Signaling Pathways to Suppress Neuroinflammation in LPS-Stimulated Mice

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