Evidence map›Paper›PMID 31103039›Full record

ReviewJournal of neuroinflammation2019

Hydrogen-rich saline promotes microglia M2 polarization and complement-mediated synapse loss to restore behavioral deficits following hypoxia-ischemic in neonatal mice via AMPK activation.

Xili Chu, Lili Cao, Zhuoya Yu, Danqing Xin, Tingting Li, Weiwei Ma, Xin Zhou, Wenqiang Chen, Dexiang Liu, Zhen Wang

Open access · goldAbstract readReview
In one paragraph

Review in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 83 citations in OpenAlex.

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  19. Nanoparticulate MgHJournal of neuroinflammation · 2023
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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

10 authors at 2 institutions in 1 country.

Xili ChuDepartment of Physiology, Shandong University School of Basic Medical Sciences, 44 Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Lili CaoDepartment of Physiology, Shandong University School of Basic Medical Sciences, 44 Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Zhuoya YuDepartment of Physiology, Shandong University School of Basic Medical Sciences, 44 Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Danqing XinDepartment of Physiology, Shandong University School of Basic Medical Sciences, 44 Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Tingting LiDepartment of Physiology, Shandong University School of Basic Medical Sciences, 44 Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Weiwei MaDepartment of Physiology, Shandong University School of Basic Medical Sciences, 44 Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Xin ZhouDepartment of Physiology, Shandong University School of Basic Medical Sciences, 44 Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Wenqiang ChenShandong University Qilu Hospital, Jinan, Shandong, People's Republic of China.
Dexiang LiuDepartment of Medical Psychology, Shandong University School of Basic Medical Sciences, 44 Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
Zhen WangDepartment of Physiology, Shandong University School of Basic Medical Sciences, 44 Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China. wangzhen@sdu.edu.cn.ORCID http://orcid.org/0000-0003-3173-6961
Shandong University · CNQilu Hospital of Shandong University · CN

Funding

Key Research and Development Foundation of Shandong Province No.2017GSF218091national key project of chronic non-communicable disease of China No.2016YFC1300403National Natural Science Foundation of China No.81770436National Natural Science Foundation of China No. 81873768 and 81671213Natural Science Foundation of Shandong Province No. ZR2016HM33
6 · The paper itself

Abstract

backgroundHypoxia-ischemia (HI) during the perinatal period is one of the most common causes of acute mortality and chronic neurologic morbidity. Hydrogen-rich saline (HS) treatment in neonatal mice has been reported to alleviate brain injury following HI, but the mechanisms involved are not known.

methodsA modified version of the Rice-Vannucci method for the induction of neonatal HI brain injury was performed on postnatal day 7 mouse pups. Animals or BV2-cells received HS and an AMPK inhibitor at indicative time post-injury.

resultsIn the current study, we show that HS treatment attenuated the accumulation of CD11b

conclusionsThese results demonstrate that HS restored behavioral deficits after HI in neonatal mice. These beneficial effects, in part, involve promoting microglia M2 polarization and complement-mediated synapse loss via AMPK activation.

Indexed as

AMP-Activated Protein KinasesAnimalsAnimals, NewbornBrainCell LineCell PolarityComplement System ProteinsEnzyme ActivationFemaleHydrogenHypoxia-Ischemia, BrainMaleMaze LearningMiceMice, Inbred C57BLMicrogliaAMP-Activated Protein KinasesComplement System ProteinsHydrogenSaline SolutionComplementHydrogen-rich salineHypoxia-ischemiaM2 polarizationSynapse loss

Identifiers

PMID31103039
PMCPMC6525972
OpenAlexW2945055038

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.