Effect of dexmedetomidine on overall Survival in Colorectal Cancer Patients
Ontology highlight
ABSTRACT:
DISEASE(S): Colorectal Cancer
PROVIDER: 41480 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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Project description:Dexmedetomidine (DEX) was served to controlling the over-reactive inflammatory effects to protect from the sepsis-induced organ failure via modulating histone methylation. However, the genome-wide changes of histone methylations upon DEX for sepsis treatment were poorly explored. (AKI) mouse model was induced by lipopolysaccharide (LPS), and added DEX (AKI+D) and KDM5A-IN-1 (KDM5A inhibitor) (AKI+K) respectively. ChIP-seq to investigate the H3K4me3 pattern in renal cortex tissues. Each group has two replications.
2020-07-03 | E-MTAB-8133 | biostudies-arrayexpress
Project description:Ischemic stroke poses a significant global health burden, with rapid revascularization treatments being crucial but often insufficient to mitigate ischemia-reperfusion (I/R) injury. Dexmedetomidine (DEX) has shown promise in reducing cerebral I/R injury, but its potential molecular mechanism, particularly its interaction with non-coding RNAs (ncRNAs), remains unclear. This study investigates DEX's therapeutic effect and potential molecular mechanisms in reducing cerebral I/R injury. A transient middle cerebral artery obstruction (tMACO) model was established to simulate cerebral I/R injury in adult rats. DEX was administered pre-ischemia and post-reperfusion. RNA sequencing and bioinformatic analyses were performed on the ischemic cerebral cortex to identify differentially expressed non-coding RNAs (ncRNAs) and mRNAs. The sequencing results showed 6494 differentially expressed (DE) mRNA and 2698 DE circRNA between the sham (S) and tMCAO (I/R) groups. Additionally, 1809 DE lncRNA, 763 DE mRNA, and 2795 DE circRNA were identified between the I/R group and tMCAO+DEX (I/R+DEX) groups. Gene ontology (GO) analysis indicated significant enrichment in multicellular biogenesis, plasma membrane components, and protein binding. KEGG analysis further highlighted the potential mechanism of DEX action in reducing cerebral I/R injury, with hub genes involved in inflammatory pathways. This study demonstrates DEX's efficacy in reducing cerebral I/R injury and offers insights into its brain-protective effects, especially in ischemic stroke. Further research is warranted to fully understand DEX's neuroprotective mechanisms and its clinical applications.
2024-07-27 | GSE268634 | GEO
Project description:Interventions: Control group (CON group):Intravenous and inhalation combined anesthesia, equal amount of normal saline; Sufentanil PCIA.;Dexmedetomidine group (DEX group):Dexmedetomidine group (DEX group): intravenous anesthesia was assisted by intravenous of DEX with the loading dose of 0.5~1.0 microgram/kg completed within 10 minutes and maintenance infusion of 0.5~1.0 microgram /kg/h until the end of the operation. Sufentanil + DEX to implement PCIA.; Epidural group (EP group):Intravenous Inhalation Combined with epidural anesthesia, ropivacaine + sufentanil PCEA;DEX + EP group:Intravenous anesthesia assisted by intravenous DEX combined with epidural anesthesia, ropivacaine + DEX PCEA.
Primary outcome(s): Peristalsis time after operation;Oral feeding time after operation
Study Design: Parallel
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Project description:Purpose: Liver tissue regeneration is vital in the restoration of liver function after hepatectomy and liver transplantation. Dexmedetomidine is a highly selective alpha2-adrenergic receptor (A2R) agonist, whichis regarded as a sedative and analgesic medication that is frequently used intra- and postoperatively in hepatic surgery. Owing to its critical role in the protection of multiple organs, the purpose of this study is to investigate the effects of dexmedetomidine on liver regeneration. Methods:Dexmedetomidine 25 μg.kg-1 was injected intraperitoneally 30 minutes before a 70% hepatectomy performed in mice. Blood and liver samples were obtained for analysis after 48 hours. Mouse primary hepatocytes (MPHMPHs) were incubated with 10 μM dexmedetomidine for 24 hours, then analyzed for cell proliferation from mRNA and protein levels. Transcriptome sequencing revealed the potential mechanism of dexmedetomidine promoting liver regeneration, verified by western blot analysis. Loss of function analysis was performed using the selective corresponding antagonist of Dexmedetomidine . Results:25 μg.kg-1 Ddexmedetomidine significantly promoted mouse liver regeneration in vivo. The liver/body weight ratio was elevated following dexmedetomidine preconditiontreatment. ImmunohistochemistryProliferative markers of Ki67, PCNA and cyclin-D1 suggested more hepatocytes enter a state of proliferatimore cell proliferationon in dexmedetomidine group via immunohistochemistry. These effects were also phenocopied in vitro Incubating withwhere 10 µM dexmedetomidine increased MPH proliferation in vitro, detected by Edu and Ki67 immunofluorescence staining. The expression of cyclins, PCNA mRNA, protein expression levels of cyclins and PCNA were higher with dexmedetomidine treatment in vivo and in vitro. The p-AKT, p-GSK3beta and beta-catenin expression levels were elevated by dexmedetomidine. The effect of dexmedetomidine on MPH proliferation and p-AKT, p-GSK3beta and beta-catenin expressionse phenomenon was blocked by atipamezole (ATI, alpha2 adrenoceptor antagonist) pretreatment. Conclusion:Dexmedetomidine activates AKT/GSK3beta/beta-catenin pathway to promote enhance liver regeneration via binding the alpha-2 adrenoreceptor, which would shed light on a potential therapeutic clinical role to protect liver function in a broad of hepatic surgery.
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2025-10-09 | GSE215154 | GEO
Project description:Background Post-traumatic stress disorder (PTSD) is a common mental disorder for which effectiveinterventions remain limited. Therefore, we set out to study whether anestheticdexmedetomidine could mitigate fear memory consolidation, part of PTSD, in mice andexplored underlying mechanisms. Methods Adult C57BL/6 male mice received dexmedetomidine (40 μg kg-1, i.p.) immediately following fear conditioning. An auditory-cued memory test in a different context wasconducted next day. RNA sequencing and neuromolecular analyses of prelimbicprefrontal cortex were performed. Molecular pathways were validated using specific gene knockdown, coupled with detailed phenotype analysis. Results Dexmedetomidine significantly reduced freezing time in mice during the auditory-cued memory test compared to control condition (15 [11.73] % vs. 59.67 [14.46] %,P=0.0018) and decreased concentrations of synaptic-related proteins (10.69 [1.27]vs. 7.97 [1.29], P<0.0001) and levels of dendritic spine density. Additionally, dexmedetomidine alleviated anxiety-like behavior and sensorimotor gating function impairment in mice after fear conditioning. These effects correlated with reduced nuclear translocation of sterol regulatory element-binding protein 1 (Srebf1) in astrocytes, but not neurons nor microglia, within the prelimbic prefrontal cortex of mice, leading to downregulation of phosphoglycerate dehydrogenase (Phgdh), a downstream target gene. Specific knockdown of Srebf1 or Phgdh in astrocytes without the treatment of dexmedetomidine inhibited fear memory consolidation and the associated synaptic plasticity in mice. Conclusions Dexmedetomidine mitigated PTSD-like behavior in mice by inhibiting fear memory consolidation through the astrocyte-specific Srebf1-Phgdh pathway in the prelimbic prefrontal cortex. These findings will promote more research toward to understanding of using anesthetic to treat PTSD and the underlying mechanism
2025-03-01 | GSE290477 | GEO
Project description:To investigate the cardioprotection of Dexmedetomidine, we established myocardial ischemia/reperfusion models in mice with vehicle or Dexmedetomidine pretreatment. We then performed mRNA sequencing of cardiac tissues and conducted gene expression profiling analysis.
2023-02-01 | GSE210873 | GEO
Project description:RNA sequencing was performed to characterize transcriptomic changes associated with dexmedetomidine treatment in MLE-12 mouse lung epithelial cells subjected to hypoxia/reoxygenation. Differential expression and functional enrichment analyses were used to identify genes and pathways potentially involved in the protective and anti-ferroptotic effects of dexmedetomidine.
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Project description:Using the highly sensitive miRNA array, we screened 83 microRNAs abundant in the myocardium and we explored the functions of these miRNAs by Gene Ontology and Kyoto Encyclopedia of Genes annotation. The enrichment results indicated that these miRNAs mainly participated in the phosphatidylinositol signaling system, PI3K-Akt, and MAPK. Furthermore, the TTC staining results showed that dexmedetomidine preconditioning attenuates myocardial ischemia-reperfusion injury by desregulation of several miRNAs and their potential target genes, which will give new insights into disclosing the mechanism of dexmedetomidine-induced cardioprotection.
2021-12-31 | GSE178505 | GEO
Project description:A significant number of liver biopsies originate from surgery or surgical resection, performed under general anaesthesia, where glucocorticoids, often dexamethasone (DEX), are routinely used as prophylaxis against postoperative nausea and vomiting (PONV) and administered perioperatively. DEX is a potent agonist of the ubiquitously expressed glucocorticoid receptor (GR), rapidly regulating transcription of hundreds of metabolic and inflammatory related genes within 0.5–2 hours of administration. Consequently, the timing and dosing of DEX administration during intraoperative liver biopsy has the potential to profoundly influence gene expression across several cell types and, thus, potentially introduce significant bias in transcriptomic analyses and mask or enhance potential biological effects. To investigate how different biopsy procedures (e.g. preoperative and intraoperative) impact transcriptomes, we performed RNA sequencing on paired liver biopsies from donors at risk of MASLD and enrolled for weight-loss surgery. This included a preoperative percutaneous baseline biopsy and an intraoperative laparoscopic biopsy obtained during weight-loss surgery. To specifically test for DEX effects on surgical biopsies, donors were administered DEX either during induction of anaesthesia or following biopsy collection. Collectively, our results indicate a clear effect of DEX on gene expression analysis of surgical liver and adipose biopsies. As exemplified by the expression of anti-inflammatory genes and the correlative analysis of liver fibrosis, we show that this can confound transcriptomic analysis and mask correlations between gene expression and biomarkers.
2026-10-02 | GSE320593 | GEO