Evidence map›Paper›PMID 35419167›Full record

ArticleOxidative medicine and cellular longevity2022

Activation of LRP6 with HLY78 Attenuates Oxidative Stress and Neuronal Apoptosis via GSK3

Peng Jin, Dongqing Qi, Yuhui Cui, Cameron Lenahan, Shuixiang Deng, Xiaogen Tao

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-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

12 citing papers in PubMed, 13 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 3 institutions in 1 country.

Peng JinDepartment of Intensive Care Unit, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, China.ORCID https://orcid.org/0000-0001-5315-4343
Dongqing QiDepartment of Rehabilitation Medicine, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, China.
Yuhui CuiDepartment of Neurosurgery, Sixth People's Hospital Affiliated to Shanghai Jiao Tong University, Shanghai 200040, China.
Cameron LenahanBurrell College of Osteopathic Medicine, Las Cruces, NM 88003, USA.
Shuixiang DengDepartment of Intensive Care Unit, Huashan Hospital, Fudan University, Shanghai 200040, China.ORCID https://orcid.org/0000-0001-5460-7279
Xiaogen TaoDepartment of Intensive Care Unit, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, China.ORCID https://orcid.org/0000-0002-0959-8876
University of Science and Technology of China · CNFudan University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Oxidative stress and neuronal apoptosis have important roles in the pathogenesis after intracerebral hemorrhage (ICH). Previous studies have reported that low-density lipoprotein receptor-related protein 6 (LRP6) exerts neuroprotection in several neurological diseases. Herein, we investigate the role of LRP6 receptor activation with HLY78 to attenuate oxidative stress and neuronal apoptosis after ICH, as well as the underlying mechanism. Methods: A total of 199 CD1 mice were used. ICH was induced via injection of autologous blood into the right basal ganglia. HLY78 was administered via intranasal injection at 1 h after ICH. To explore the underlying mechanism, LRP6 siRNA and selisistat, a Sirt1 selective antagonist, were injected intracerebroventricularly at 48 h before ICH induction. Neurobehavioral tests, Western blot, and immunofluorescence staining were performed. Results: The expression of endogenous p-LRP6 was gradually increased and expressed on neurons after ICH. HLY78 significantly improved the short- and long-term neurobehavioral deficits after ICH, which was accompanied with decreased oxidative stress and neuronal apoptosis, as well as increased expression of p-GSK3 Conclusion: Our results suggest that administration of HLY78 attenuated oxidative stress, neuronal apoptosis, and neurobehavioral impairments through the LRP6/GSK3

Indexed as

Cerebral HemorrhageLow Density Lipoprotein Receptor-Related Protein-6Oxidative StressSirtuin 1AnimalsApoptosisBenzodioxolesGlycogen Synthase Kinase 3 betaMicePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhenanthridines4-ethyl-5-methyl-5,6-dihydro(1,3)dioxolo(4,5-j)phenanthridineBenzodioxolesGlycogen Synthase Kinase 3 betaLow Density Lipoprotein Receptor-Related Protein-6Lrp6 protein, mousePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhenanthridinesSirt1 protein, mouseSirtuin 1

Identifiers

PMID35419167
PMCPMC9001077
OpenAlexW4226083030

What OpenQuestion holds

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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.