Evidence map›Paper›PMID 31638230›Full record

ArticleMolecular medicine reports2019

Theaflavin attenuates cerebral ischemia/reperfusion injury by abolishing miRNA‑128‑3p‑mediated Nrf2 inhibition and reducing oxidative stress.

Ronggang Li, Xin Li, Haibing Wu, Zhikun Yang, Li Fei, Jianhong Zhu

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

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
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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 4 institutions in 1 country.

Ronggang LiDepartment of Neurosurgery, Fudan University Huashan Hospital and State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai 200040, P.R. China.
Xin LiDepartment of Imaging, Jinshan Hospital Affiliated to Fudan University, Shanghai 201508, P.R. China.
Haibing WuShanghai Public Health Clinical Center, Fudan University, Shanghai 201508, P.R. China.
Zhikun YangDepartment of Neurosurgery, Jinshan Hospital Affiliated to Fudan University, Shanghai 201508, P.R. China.
Li FeiDepartment of Neurosurgery, Jinshan Hospital Affiliated to Fudan University, Shanghai 201508, P.R. China.
Jianhong ZhuDepartment of Neurosurgery, Fudan University Huashan Hospital and State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai 200040, P.R. China.
Jinshan Hospital of Fudan University · CNFudan University · CNHuashan Hospital · CNShanghai Public Health Clinical Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Theaflavin has been proven to own strong antioxidative capacity; however, the molecular mechanism underlying its protective effect against cerebral ischemia‑reperfusion (I/R) injury remains unclear. Therefore, the present study was designed to elucidate the neuroprotective effects of theaflavin on cerebral I/R injury and its underlying molecular mechanisms. To investigate the effects of theaflavin on neurological function, neurogenesis, and oxidative stress, experiments were performed using a cerebral I/R injury rat model, and neural stem cells (NSCs) were subjected to oxygen‑glucose deprivation and reoxygenation (OGD/R). Further, the expression profiles of miRNA‑128‑3p and the regulatory function of nuclear factor (erythroid‑derived 2)‑related factor 2 (Nrf2) were evaluated in these models. We found that theaflavin treatment significantly reduced infarct volume and neuronal injury, and thus improved the impaired memory and learning ability. Furthermore, theaflavin treatment significantly enhanced the increase in NSC proliferation, reduction in the apoptotic rate and inhibition of oxidative stress. Mechanistically, theaflavin targeted miRNA‑128‑3p and further activated the Nrf2 pathway to reduce oxidative stress. In summary, theaflavin has a strong ability to attenuate cerebral I/R injury through miRNA‑128‑3p‑mediated recovery of the impaired antioxidant defense system, which suggests that it could be a potential drug candidate for ischemic stroke.

Indexed as

AnimalsAntioxidantsBiflavonoidsBrain IschemiaCatechinCells, CulturedGene Expression RegulationMaleMicroRNAsNeuroprotective AgentsNF-E2-Related Factor 2Oxidative StressRatsRats, Sprague-DawleyReperfusion InjuryAntioxidantsBiflavonoidsCatechinMicroRNAsMIRN128 microRNA, ratNeuroprotective AgentsNF-E2-Related Factor 2theaflavin

Identifiers

PMID31638230
PMCPMC6854549
OpenAlexW2980552495

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.