Dexmedetomidine post-conditioning attenuates cerebral ischemia following asphyxia cardiac arrest through down-regulation of apoptosis and neuroinflammation in rats

Li, Guangqian; LeiQian,; Gu, Pan; Fan, Dan

doi:10.1186/s12871-021-01394-7

Cited by 5 publications

(1 citation statement)

References 45 publications

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“…Previous studies have shown that ischemia/reperfusion injury to the central nervous system can lead to the activation of inflammatory factors, which induces the release of pro-inflammatory factors and chemokines that exacerbate the inflammatory response and ultimately lead to neuronal death [ 29 ]. A biochemical analysis of acute myocardial infarction identified IL1B as a biomarker of acute myocardial infarction that mediates the inflammatory response after acute myocardial infarction [ 30 – 32 ]. These studies are consistent with the present study, indicating that IL1B can participate in the biological process after ischemia-reperfusion injury in cardiovascular and cerebrovascular diseases, thereby changing the endpoint of cardiovascular and cerebrovascular disease events.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics and experimental analyses of glutamate receptor and its targets genes in myocardial and cerebral ischemia

Liao

Yang

et al. 2023

BMC Genomics

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Background There is a mutual hemodynamic and pathophysiological basis between the heart and brain. Glutamate (GLU) signaling plays an important role in the process of myocardial ischemia (MI) and ischemic stroke (IS). To further explore the common protective mechanism after cardiac and cerebral ischemic injuries, the relationship between GLU receptor-related genes and MI and IS were analyzed. Results A total of 25 crosstalk genes were identified, which were mainly enriched in the Toll-like receptor signaling pathway, Th17 cell differentiation, and other signaling pathways. Protein-protein interaction analysis suggested that the top six genes with the most interactions with shared genes were IL6, TLR4, IL1B, SRC, TLR2, and CCL2. Immune infiltration analysis suggested that immune cells such as myeloid-derived suppressor cells and monocytes were highly expressed in the MI and IS data. Memory B cells and Th17 cells were expressed at low levels in the MI and IS data; molecular interaction network construction suggested that genes such as JUN, FOS, and PPARA were shared genes and transcription factors; FCGR2A was a shared gene of MI and IS as well as an immune gene. Least absolute shrinkage and selection operator logistic regression analysis identified nine hub genes: IL1B, FOS, JUN, FCGR2A, IL6, AKT1, DRD4, GLUD2, and SRC. Receiver operating characteristic analysis revealed that the area under the curve of these hub genes was > 65% in MI and IS for all seven genes except IL6 and DRD4. Furthermore, clinical blood samples and cellular models showed that the expression of relevant hub genes was consistent with the bioinformatics analysis. Conclusions In this study, we found that the GLU receptor-related genes IL1B, FOS, JUN, FCGR2A, and SRC were expressed in MI and IS with the same trend, which can be used to predict the occurrence of cardiac and cerebral ischemic diseases and provide reliable biomarkers to further explore the co-protective mechanism after cardiac and cerebral ischemic injury.

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Section: Discussionmentioning

confidence: 99%

Bioinformatics and experimental analyses of glutamate receptor and its targets genes in myocardial and cerebral ischemia

Liao

Yang

et al. 2023

BMC Genomics

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Dexmedetomidine improves oxygen-glucose deprivation/reoxygenation (OGD/R) -induced neurological injury through regulating SNHG11/miR-324-3p/VEGFA axis

Chen

Fan

2021

Bioengineered

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Dexmedetomidine (Dex) has been reported to exhibit neuroprotective effects through various regulatory mechanisms. This study aims to investigate the role and molecular mechanism of SNHG11 in Dex-mediated neuroprotection. The ischemic stroke (IS) model was established in vivo by middle cerebral artery occlusion (MCAO) and in vitro by oxygen-glucose deprivation and reperfusion (OGD/R)-treated SH-SY5Y. SNHG11 was highly expressed after OGD/R, and Dex improved OGD/R-induced neurological injury. Additionally, Dex reversed the effects of SNHG11 on OGD/R-induced neurological injury. Furthermore, we found that SNHG11 upregulated vascular endothelial growth factor A (VEGFA) expression by targeting miR-324-3p. Through rescue assays, it was confirmed that SNHG11 regulated OGD/R-induced neurological injury through increasing VEGFA expression. At last, Dex was also discovered to improve neurological injury through regulating SNHG11 in the rat model. In conclusion, our work demonstrated that Dex improved OGD/R-induced neurological injury via SNHG11/miR-324-3p/VEGFA axis. These findings may offer a novel therapeutic strategy for IS treatment.

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Dexmedetomidine mitigates neuroinflammation and improves early postoperative neurocognitive dysfunction in rats by enhancing autophagy

Wang

Xin

Chu

et al. 2023

Journal of Neurophysiology

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Postoperative neurocognitive dysfunction (PND) is a common postoperative complication. Autophagy is correlated with the pathogenesis of PND. This study investigated the potential role of autophagy in the neuroprotection of Dexmedetomidine (Dex) pretreatment in PND. The PND rat model was established by abdominal surgery. The cognitive function of rats was evaluated by Y-maze 3 days after surgery. Nissl staining assessed postoperative hippocampal damage. Immunofluorescence detected the expression of microglial activation (Iba-1) and autophagy-related protein (LC3B) in hippocampal tissues. Western blot detected the autophagy-related protein expression (Beclin 1, LC3B, and p62), proinflammatory cytokines, and the protein activation of the LKB1/AMPK/ULK-1 signaling pathway. RT-PCR quantified the expression of IL-1β, TNF-α, and IL6. In this study, we found Dex pretreatment improved spatial memory function impairment and reduced abdominal surgery-induced hippocampal tissue damage. Dex pretreatment significantly increased the expression of Beclin 1 and LC3 II/I, and decreased the expression of p62 in the hippocampus after surgery. Furthermore, Dex effectively inhibited microglial activation and proinflammatory cytokines by enhancing autophagy in the hippocampus. Pretreatment with 3-MA, an autophagy inhibitor, the inhibitory effect of Dex on postoperative neuroinflammation was significantly weakened. We further demonstrated that Dex suppressed surgery-induced neuroinflammation by activating the LKB/AMPK/ULK1 signaling pathway. In conclusion, our study indicated that Dex inhibited hippocampal neuroinflammation and ameliorated PND by enhancing autophagy after surgery in rats, which was related to the LKB1/AMPK/ULK1 signaling pathway. These findings provide a potential therapeutic prospect for PND.

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Dexmedetomidine post-conditioning attenuates cerebral ischemia following asphyxia cardiac arrest through down-regulation of apoptosis and neuroinflammation in rats

Cited by 5 publications

References 45 publications

Bioinformatics and experimental analyses of glutamate receptor and its targets genes in myocardial and cerebral ischemia

Bioinformatics and experimental analyses of glutamate receptor and its targets genes in myocardial and cerebral ischemia

Dexmedetomidine improves oxygen-glucose deprivation/reoxygenation (OGD/R) -induced neurological injury through regulating SNHG11/miR-324-3p/VEGFA axis

Dexmedetomidine mitigates neuroinflammation and improves early postoperative neurocognitive dysfunction in rats by enhancing autophagy

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