Evidence map›Paper›PMID 31746402›Full record

ArticleMolecular medicine reports2020

Sevoflurane attenuates brain damage through inhibiting autophagy and apoptosis in cerebral ischemia‑reperfusion rats.

Cun-Xian Shi, Jin Jin, Xue-Qin Wang, Teng Song, Guang-Hong Li, Ke-Zhong Li, Jia-Hai Ma

RetractedOpen access · hybridAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 56 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

Cun-Xian Shi *Department of Anesthesiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, P.R. China.
Jin Jin *Department of Anesthesiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, P.R. China.
Xue-Qin WangDepartment of Anesthesiology, Linyi People's Hospital, Linyi, Shandong 276000, P.R. China.
Teng SongDepartment of Neurosurgery, Heze Municipal Hospital, Heze, Shandong 274000, P.R. China.
Guang-Hong LiDepartment of Neurosurgery, Heze Municipal Hospital, Heze, Shandong 274000, P.R. China.
Ke-Zhong LiDepartment of Anesthesiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, P.R. China.
Jia-Hai MaDepartment of Anesthesiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, P.R. China.
Yuhuangding Hospital · CNHeze Municipal Hospital · CNLinyi People's Hospital · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aimed to investigate the effects of sevoflurane post‑conditioning in a rat brain cerebral ischemia‑reperfusion (I/R) model and examine its possible mechanism. Rats were randomly divided into six groups: Sham control group (Sham), I/R group, sevoflurane group (Se), Toll‑like receptor‑4 (TLR4) inhibitor group (Tak‑242), nuclear factor (NF)‑κB inhibitor group (QNZ) and Sevoflurane post‑conditioning combined with TLR4‑NF‑κB signaling pathway inhibitor group (Se + Tak‑242). Morris water maze test and tetrazolium chloride staining were used to investigate the I/R injury. The nerve cell apoptosis and autophagy in cortical tissue were detected by TUNEL and transmission electron microscopy, respectively. The expression of TLR4 protein in cortical tissue was observed by immunohistochemical staining. The expression of autophagy and apoptotic associated proteins in cortical tissues and the activity of TLR4‑NF‑κB signaling pathway were assayed by western blot analysis. Sevoflurane post‑conditioning improved the learning and memory dysfunction caused by cerebral I/R injury. The cerebral infarction area, nerve cell apoptosis and formation of autophagic vacuoles were reduced after sevoflurane administration. The expression of light chain 3II/I, Beclin‑1, Bad and Cleaved‑Caspase‑3 proteins were inhibited and the expression of Bcl‑2 protein was upregulated after sevoflurane administration. Sevoflurane post‑conditioning also inhibited the TLR4 protein and NF‑κB phosphorylation, and increased inhibitor of kBα phosphorylation. The treatment effect of Tak‑242 and QNZ groups were not significantly different compared with the Se group (P>0.05), and the Se + Tak‑242 group had the best results. The present study demonstrated that sevoflurane post‑conditioning could protect middle cerebral artery occlusion‑induced brain injury rats by inhibiting autophagy and apoptosis, and that its mechanism is related to the TLR4‑NF‑κB signaling pathway.

Indexed as

AnimalsApoptosisCerebral CortexDisease Models, AnimalMaleNeuronsRatsRats, Sprague-DawleyReperfusion InjurySevofluraneSignal TransductionSevofluraneapoptosisautophagycerebral ischemia-reperfusion injurysevofluraneToll-like receptor-4-nuclear factor-κB

Identifiers

PMID31746402
PMCPMC6896401
OpenAlexW2991052421

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.