Evidence map›Paper›PMID 32482998›Full record

ArticleAnesthesiology2020

Dexmedetomidine Exerts an Anti-inflammatory Effect via α2 Adrenoceptors to Prevent Lipopolysaccharide-induced Cognitive Decline in Mice.

Rong Li, Ieng K Lai, Jonathan Z Pan, Pengbo Zhang, Mervyn Maze

Open access · greenAbstract readComment
In one paragraph

Article in Anesthesiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.

  1. Appraisal of the Neuroprotective Effect of Dexmedetomidine: A Meta-Analysis.Advances in experimental medicine and biology · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Rong LiFrom the Department of Anesthesiology, Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China (R.L., P.Z.) the Center for Brain Science, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China (R.L.) the Center for Cerebrovascular Research, Department of Anesthesia and Perioperative Care (R.L., I.K.L., J.Z.P., M.M.) the Brain and Spinal Injury Center (J.Z.P.), University of California, San Francisco, California.
Ieng K Lai
Jonathan Z Pan
Pengbo Zhang
Mervyn Maze
Second Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

Inflammation resolving mechanism dysregulation in postoperative cognitive declineR01GM104194 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MAZE, MERVYN · 2013 to 2016
$1.2M
NIGMS NIH HHS R01 GM104194
6 · The paper itself

Abstract

backgroundClinical studies have shown that dexmedetomidine ameliorates cognitive decline in both the postoperative and critical care settings. This study determined the mechanism(s) for the benefit provided by dexmedetomidine in a medical illness in mice induced by lipopolysaccharide.

methodsCognitive decline, peripheral and hippocampal inflammation, blood-brain barrier permeability, and inflammation resolution were assessed in male mice. Dexmedetomidine was administered in the presence of lipopolysaccharide and in combination with blockers. Cultured macrophages (RAW 264.7; BV-2) were exposed to lipopolysaccharide ± dexmedetomidine ± yohimbine; tumor necrosis factor α release into the medium and monocyte NFκB activity was determined.

resultsIn vivo, lipopolysaccharide-induced cognitive decline and inflammation (mean ± SD) were reversed by dexmedetomidine (freezing time, 55.68 ± 12.31 vs. 35.40 ± 17.66%, P = 0.0286, n = 14; plasma interleukin [IL]-1β: 30.53 ± 9.53 vs. 75.68 ± 11.04 pg/ml, P < 0.0001; hippocampal IL-1β: 3.66 ± 1.88 vs. 28.73 ± 5.20 pg/mg, P < 0.0001; n = 8), which was prevented by α2 adrenoceptor antagonists. Similar results were found in 12-month-old mice. Lipopolysaccharide also increased blood-brain barrier leakage, inflammation-resolution orchestrator, and proresolving and proinflammatory mediators; each lipopolysaccharide effect was attenuated by dexmedetomidine, and yohimbine prevented dexmedetomidine's attenuating effect. In vitro, lipopolysaccharide-induced tumor necrosis factor α release (RAW 264.7: 6,308.00 ± 213.60 vs. 7,767.00 ± 358.10 pg/ml, P < 0.0001; BV-2: 1,075.00 ± 40.41 vs. 1,280.00 ± 100.30 pg/ml, P = 0.0003) and NFκB-p65 activity (nuclear translocation [RAW 264.7: 1.23 ± 0.31 vs. 2.36 ± 0.23, P = 0.0031; BV-2: 1.08 ± 0.26 vs. 1.78 ± 0.14, P = 0.0116]; phosphorylation [RAW 264.7: 1.22 ± 0.40 vs. 1.94 ± 0.23, P = 0.0493; BV-2: 1.04 ± 0.36 vs. 2.04 ± 0.17, P = 0.0025]) were reversed by dexmedetomidine, which was prevented by yohimbine.

conclusionsPreclinical studies suggest that the cognitive benefit provided by dexmedetomidine in mice administered lipopolysaccharide is mediated through α2 adrenoceptor-mediated anti-inflammatory pathways.

Indexed as

Cognitive DysfunctionDexmedetomidineAnimalsAnti-Inflammatory AgentsCritical IllnessLipopolysaccharidesMaleMiceReceptors, AdrenergicRodentiaTumor Necrosis Factor-alphaAnti-Inflammatory AgentsDexmedetomidineLipopolysaccharidesReceptors, AdrenergicTumor Necrosis Factor-alpha

Identifiers

PMID32482998
PMCPMC12902830
OpenAlexW3028934650

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.