Evidence map›Paper›PMID 33708336›Full record

ArticleOxidative medicine and cellular longevity2021

Albumin Reduces Oxidative Stress and Neuronal Apoptosis via the ERK/Nrf2/HO-1 Pathway after Intracerebral Hemorrhage in Rats.

Shuixiang Deng, Shengpeng Liu, Peng Jin, Shengjie Feng, Mi Tian, Pengju Wei, Hongda Zhu, Jiaying Tan, Feng Zhao, Ye Gong

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.7field-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

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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

42 citing papers in PubMed, 61 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

10 authors at 2 institutions in 1 country.

Shuixiang DengDepartment of Critical Care Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.ORCID https://orcid.org/0000-0001-5460-7279
Shengpeng LiuDepartment of Pediatrics, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, Shenzhen, Guangdong, China.
Peng JinDepartment of Critical Care Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.
Shengjie FengDepartment of Critical Care Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.
Mi TianDepartment of Critical Care Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.
Pengju WeiState Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai 200032, China.
Hongda ZhuDepartment of Neurosurgery, Huashan Hospital, Fudan University, Shanghai 200040, China.
Jiaying TanDepartment of Critical Care Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.
Feng ZhaoDepartment of Critical Care Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.
Ye GongDepartment of Critical Care Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.ORCID https://orcid.org/0000-0002-9531-0946
Fudan University · CNJinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlbumin has been regarded as a potent antioxidant with free radical scavenging activities. Oxidative stress and neuronal apoptosis are responsible for its highly damaging effects on brain injury after intracerebral hemorrhage (ICH). Here, the present study investigated the neuroprotective effect of albumin against early brain injury after ICH and the potential underlying mechanisms.

methodsAdult male Sprague-Dawley rats were subjected to intrastriatal injection of autologous blood to induce ICH. Human serum albumin was given by intravenous injection 1 h after ICH. U0126, an inhibitor of extracellular signal-regulated kinase (ERK1/2), and ML385, an inhibitor of nuclear factor-E2-related factor 2 (Nrf2), were intraperitoneally administered 1 h before ICH induction. Short- and long-term neurobehavioral tests, western blotting, immunofluorescence staining, oxidative stress evaluations, and apoptosis measurements were performed.

resultsEndogenous expression of albumin (peaked at 5 days) and heme oxygenase 1 (HO-1, peaked at 24 h) was increased after ICH compared with the sham group. Albumin and HO-1 were colocalized with neurons. Compared with vehicle, albumin treatment significantly improved short- and long-term neurobehavioral deficits and reduced oxidative stress and neuronal death at 72 h after ICH. Moreover, albumin treatment significantly promoted the phosphorylation of ERK1/2; increased the expression of Nrf2, HO-1, and Bcl-2; and downregulated the expression of Romo1 and Bax. U0126 and ML385 abolished the treatment effects of albumin on behavior and protein levels after ICH.

conclusionsAlbumin attenuated oxidative stress-related neuronal death may in part via the ERK/Nrf2/HO-1 signaling pathway after ICH in rats. Our study suggests that albumin may be a novel therapeutic method to ameliorate brain injury after ICH.

Indexed as

AnimalsApoptosisCerebral HemorrhageHeme Oxygenase-1HumansMaleMAP Kinase Signaling SystemMemoryMotor ActivityNerve DegenerationNeuronsNF-E2-Related Factor 2Oxidative StressRatsRats, Sprague-DawleySerum Albumin, HumanHeme Oxygenase-1NF-E2-Related Factor 2Serum Albumin, Human

Identifiers

PMID33708336
PMCPMC7932792
OpenAlexW3130225263

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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.