Evidence map›Paper›PMID 36367210›Full record

ArticleBioscience reports2022

Leptin alleviates endoplasmic reticulum stress induced by cerebral ischemia/reperfusion injury via the PI3K/Akt signaling pathway.

Yan Zhang, Daobin Cheng, Chunxiao Jie, Tao Liu, Shixiong Huang, Shijun Hu

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In one paragraph

Article in Bioscience reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Yan ZhangDepartment of Rehabilitation, The Second Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530007, People's Republic of China.
Daobin ChengDepartment of Neurology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Chunxiao JieDepartment of Neurology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Tao LiuDepartment of Neurology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, Hainan 570311, People's Republic of China.
Shixiong HuangDepartment of Neurology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, Hainan 570311, People's Republic of China.
Shijun HuDepartment of Neurology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, Hainan 570311, People's Republic of China.ORCID 0000-0002-1497-344X
Guangxi Medical University · CNHainan General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCerebral ischemic/reperfusion injury (CIRI) is a key factor for the prognosis of ischemic stroke (IS), the leading disease in terms of global disability and fatality rates. Recent studies have shown that endoplasmic reticulum stress (ERS) may be a target against CIRI and that leptin, a peptide hormone, has neuroprotective activity to mitigate CIRI.

methodsAn in vitro CIRI model was induced in primary cortical neurons by oxygen-glucose deprivation and reoxygenation (OGD/R) after pretreatment with LY294002 (10 µmol/L) and/or leptin (0.4 mg/L), and cell viability, neuronal morphology and endoplasmic reticulum (ER) dysfunction were evaluated. An in vivo CIRI model was established in rats by middle cerebral artery occlusion and reperfusion (MCAO/R) after the injection of LY294002 (10 μmol/L) and/or leptin (1 mg/kg), and neurological function, infarct volume, cerebral pathological changes, the expression of ERS-related proteins and cell apoptosis were examined.

resultsIn vitro, leptin treatment improved the cell survival rate, ameliorated neuronal pathological morphology and alleviated OGD/R-induced ERS. In vivo, administration of leptin significantly reduced the infarct volume, neurological deficit scores and neuronal apoptosis as well as pathological alterations. In addition, leptin suppressed MCAO/R-induced ERS and may decrease apoptosis by inhibiting ERS-related death and caspase 3 activation. It also regulated expression of the antiapoptotic protein Bcl-2 and the proapoptotic protein Bax in the cortex. Furthermore, the inhibitory effect of leptin on ERS was significantly decreased by the effective phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002.

conclusionsThese results confirm that ERS plays an important role in CIRI and that leptin can inhibit the activation of ERS through the PI3K/Akt pathway, thereby alleviating CIRI. These findings provide novel therapeutic targets for IS.

Indexed as

Endoplasmic Reticulum StressNeuroprotective AgentsReperfusion InjuryAnimalsApoptosisGlucoseInfarction, Middle Cerebral ArteryOxygenPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsRatsRats, Sprague-DawleySignal TransductionGlucoseNeuroprotective AgentsOxygenPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase Inhibitorscerebral ischemic/reperfusion injuryendoplasmic reticulum stressleptinPI3K/Akt signaling pathway

Identifiers

PMID36367210
PMCPMC9744719
OpenAlexW4308768581

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Registered trials

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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.