Evidence map›Paper›PMID 34180121›Full record

ArticleJournal of cellular and molecular medicine2021

Puerarin attenuates intracerebral hemorrhage-induced early brain injury possibly by PI3K/Akt signal activation-mediated suppression of NF-κB pathway.

Jun Zeng, Shizhong Zheng, Yizhao Chen, Yaoming Qu, Jiayu Xie, Enhui Hong, Hongzhu Lv, Rui Ding, Liang Feng, Zhichong Xie

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 39 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 5 institutions in 1 country.

Jun ZengDepartment of Neurosurgery, Zhujiang Hospital, The Engineering Technology Research Center of Education Ministry of China, The National Key Clinical Specialty, The Neurosurgery Institute of Guangdong Province, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Southern Medical University, Guangzhou, China.
Shizhong ZhengDepartment of Neurosurgery, Zhujiang Hospital, The Engineering Technology Research Center of Education Ministry of China, The National Key Clinical Specialty, The Neurosurgery Institute of Guangdong Province, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Southern Medical University, Guangzhou, China.
Yizhao ChenDepartment of Neurosurgery, Zhujiang Hospital, The Engineering Technology Research Center of Education Ministry of China, The National Key Clinical Specialty, The Neurosurgery Institute of Guangdong Province, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Southern Medical University, Guangzhou, China.ORCID 0000-0002-7357-9127
Yaoming QuDepartment of Radiology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Jiayu XieDepartment of Neurosurgery, Zhujiang Hospital, The Engineering Technology Research Center of Education Ministry of China, The National Key Clinical Specialty, The Neurosurgery Institute of Guangdong Province, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Southern Medical University, Guangzhou, China.
Enhui HongDepartment of Neurosurgery, Zhujiang Hospital, The Engineering Technology Research Center of Education Ministry of China, The National Key Clinical Specialty, The Neurosurgery Institute of Guangdong Province, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Southern Medical University, Guangzhou, China.
Hongzhu LvDepartment of Neurosurgery, Zhujiang Hospital, The Engineering Technology Research Center of Education Ministry of China, The National Key Clinical Specialty, The Neurosurgery Institute of Guangdong Province, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Southern Medical University, Guangzhou, China.
Rui DingDepartment of Neurosurgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Liang FengDepartment of Neurosurgery, Chenzhou No. 1 People's Hospital, Chenzhou, China.
Zhichong XieDepartment of Neurosurgery, Zhujiang Hospital, The Engineering Technology Research Center of Education Ministry of China, The National Key Clinical Specialty, The Neurosurgery Institute of Guangdong Province, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Southern Medical University, Guangzhou, China.
Zhujiang Hospital · CNSun Yat-sen University · CNChenzhou First People's Hospital · CNFirst Affiliated Hospital of Guangzhou Medical University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intracerebral hemorrhage (ICH) can induce intensively oxidative stress, neuroinflammation, and brain cell apoptosis. However, currently, there is no highly effective treatment available. Puerarin (PUE) possesses excellent neuroprotective effects by suppressing the NF-κB pathway and activating the PI3K/Akt signal, but its role and related mechanisms in ICH-induced early brain injury (EBI) remain unclear. In this study, we intended to observe the effects of PUE and molecular mechanisms on ICH-induced EBI. ICH was induced in rats by collagenase IV injection. PUE was intraperitoneally administrated alone or with simultaneously intracerebroventricular injection of LY294002 (a specific inhibitor of the PI3K/Akt signal). Neurological deficiency, histological impairment, brain edema, hematoma volume, blood-brain barrier destruction, and brain cell apoptosis were evaluated. Western blot, immunohistochemistry staining, reactive oxygen species (ROS) measurement, and enzyme-linked immunosorbent assay were performed. PUE administration at 50 mg/kg and 100 mg/kg could significantly reduce ICH-induced neurological deficits and EBI. Moreover, PUE could notably restrain ICH-induced upregulation of the NF-κB pathway, pro-inflammatory cytokines, ROS level, and apoptotic pathway and activate the PI3K/Akt signal. However, LY294002 delivery could efficaciously weaken these neuroprotective effects of PUE. Overall, PUE could attenuate ICH-induced behavioral defects and EBI possibly by PI3K/Akt signal stimulation-mediated inhibition of the NF-κB pathway, and this made PUE a potential candidate as a promising therapeutic option for ICH-induced EBI.

Indexed as

Oxidative StressAnimalsBrain InjuriesCerebral HemorrhageDisease Models, AnimalIsoflavonesMaleNeuroprotective AgentsNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleySignal TransductionVasodilator AgentsIsoflavonesNeuroprotective AgentsNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktpuerarinVasodilator AgentsEBIICHNF-κBPI3Kpuerarin

Identifiers

PMID34180121
PMCPMC8358853
OpenAlexW3177074046

What OpenQuestion 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 OpenQuestion graph.