Evidence map›Paper›PMID 32350570›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2020

Hydrogen attenuates sepsis-associated encephalopathy by NRF2 mediated NLRP3 pathway inactivation.

Keliang Xie, Yang Zhang, Yaoqi Wang, Xiaoyin Meng, Yuzun Wang, Yonghao Yu, Hongguang Chen

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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

41 citing papers in PubMed, 73 citations in OpenAlex.

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  16. Prospects of molecular hydrogen in cancer prevention and treatment.Journal of cancer research and clinical oncology · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Keliang XieDepartment of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Research Institute of Anesthesiology, NO.154 Anshan Road, Tianjin, 300052, China.
Yang ZhangDepartment of Anesthesiology, Tianjin 4th center hospital, Tianjin, 300140, China.
Yaoqi WangDepartment of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Research Institute of Anesthesiology, NO.154 Anshan Road, Tianjin, 300052, China.
Xiaoyin MengDepartment of Gynaecology and Obstetrics, Tianjin Hospital, Tianjin, 300211, China.
Yuzun WangDepartment of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Research Institute of Anesthesiology, NO.154 Anshan Road, Tianjin, 300052, China.
Yonghao YuDepartment of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Research Institute of Anesthesiology, NO.154 Anshan Road, Tianjin, 300052, China.
Hongguang ChenDepartment of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Research Institute of Anesthesiology, NO.154 Anshan Road, Tianjin, 300052, China. daguang521521@163.com.
Tianjin Medical University General Hospital · CNTianjin Hospital · CN

Funding

National Natural Science Foundation of China 81601667National Natural Science Foundation of China 81671888National Natural Science Foundation of China 81772043Natural Science Foundation of Tianjin 18JCYBJC93700Natural Science Foundation of Tianjin City 17JCYBJC24800Science and Technology Support Key Program Affiliated to the Key Research and Development Plan of Tianjin Science and Technology Project 18YFZCSY00560
6 · The paper itself

Abstract

objectiveSepsis-associated encephalopathy (SAE) is a major cause of mortality worldwide. Oxidative stress, inflammatory response and apoptosis participate in the pathogenesis of SAE. Nuclear factor erythroid 2-related factor 2 (Nrf2) and nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) pathway is involved in oxidative stress and inflammatory response. We reported that hydrogen gas protected against sepsis in wild-type (WT) but not Nrf2 knockout (KO) mice. Therefore, it is vital to identify the underlying cause of hydrogen gas treatment of sepsis-associated encephalopathy.

methodsSAE was induced in WT and Nrf2 KO mice by cecal ligation and puncture (CLP). As a NLRP3 inflammasome inhibitor, MCC950 (50 mg/kg) was administered by intraperitoneal (i.p.) injection before operation. Hydrogen gas (H

resultsSAE increased NLRP3 and Nrf2 expression in microglia. MCC950 inhibited SAE-induced NLRP3 expression, interleukin (IL)-1β and IL-18 cytokine release, neuronal apoptosis and mitochondrial dysfunction. SAE increased NLRP3 and caspase-1 expression in WT mice compared to Nrf2 KO mice. Hydrogen increased Nrf2 expression and inhibited the SAE-induced expression of NLRP3, caspase-1, cytokines IL-1β and IL-18, neuronal apoptosis, and mitochondrial dysfunction in WT mice but not Nrf2 KO mice.

conclusionSAE increased NLRP3 and Nrf2 expression in microglia. Hydrogen alleviated inflammation, neuronal apoptosis and mitochondrial dysfunction via inhibiting Nrf2-mediated NLRP3 pathway.

Indexed as

AnimalsApoptosisBrainBrain ChemistryCecumCerebral CortexCytokinesFuransHeterocyclic Compounds, 4 or More RingsHydrogenIndenesMaleMiceMice, KnockoutMicrogliaMitochondriaCytokinesFuransHeterocyclic Compounds, 4 or More RingsHydrogenIndenesN-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamideNfe2l2 protein, mouseNF-E2-Related Factor 2NLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseSulfonamidesSulfonesHydrogenNLRP3Nrf2SAE

Identifiers

PMID32350570
OpenAlexW3021044908

What OpenQuestion holds

Textmetadata
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.