Evidence map›Paper›PMID 35693707›Full record

ArticleOxidative medicine and cellular longevity2022

Hydroxytyrosol Alleviated Hypoxia-Mediated PC12 Cell Damage through Activating PI3K/AKT/mTOR-HIF-1

Xiaolin Li, Xiuyu Tian, Tianlong Liu, Maoxing Li, Weigang Wang, Peng Wang, Ziliang Guo

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
0.9field-weighted citation impact, top 31% 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, 9 citations in OpenAlex.

  1. Review
  2. Upregulation ofTranslational andrology and urology · 2026
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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

7 authors at 3 institutions in 1 country.

Xiaolin LiDepartment of Clinical Pharmacy, The 940th Hospital of Joint Logistic Support Force of Chinese People's Liberation Army, Lanzhou 730050, China.
Xiuyu TianDepartment of Clinical Pharmacy, The 940th Hospital of Joint Logistic Support Force of Chinese People's Liberation Army, Lanzhou 730050, China.
Tianlong LiuDepartment of Clinical Pharmacy, The 940th Hospital of Joint Logistic Support Force of Chinese People's Liberation Army, Lanzhou 730050, China.
Maoxing LiDepartment of Clinical Pharmacy, The 940th Hospital of Joint Logistic Support Force of Chinese People's Liberation Army, Lanzhou 730050, China.ORCID https://orcid.org/0000-0003-3684-9308
Weigang WangDepartment of Clinical Pharmacy, The 940th Hospital of Joint Logistic Support Force of Chinese People's Liberation Army, Lanzhou 730050, China.
Peng WangDepartment of Clinical Pharmacy, The 940th Hospital of Joint Logistic Support Force of Chinese People's Liberation Army, Lanzhou 730050, China.
Ziliang GuoDepartment of Clinical Pharmacy, The 940th Hospital of Joint Logistic Support Force of Chinese People's Liberation Army, Lanzhou 730050, China.
Gansu University of Traditional Chinese Medicine · CNPeople's Liberation Army 401 Hospital · CNMinzu University of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Hypoxia exerts pressure on cells and organisms, and this pressure can occur under both pathological and nonpathological conditions. There are many reports confirmed that hydroxytyrosol has good in vitro antioxidant activity, while the research about hydroxytyrosol on hypoxia-mediated cell damage is still unclear. Purpose: The aim of this study was to investigate the effect and mechanism of hydroxytyrosol on hypoxia-mediated cell damage. Methods: We studied the effects of hydroxytyrosol on the content of reactive oxygen species, the change of antioxidant enzymes activity of SOD, CAT, and GSH-Px and the content of oxidation products MDA and GSH, and the changes of cell membrane potential and effect on PI3K/AKT/mTOR-HIF-1 Results: PC12 cell treated with hydroxytyrosol abated the cell apoptosis and alleviated the oxidative stress through scavenging of reactive oxygen species, improving the enzyme activity and changing the content of oxidation products and alleviating mitochondria damage. Western blotting confirmed that the mechanism maybe related to the PI3K/AKT/mTOR-HIF-1 Conclusion: Hydroxytyrosol reduced the oxidative stress and resisted the inhibition of PI3K/AKT/mTOR-HIF-1

Indexed as

Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAnimalsCell HypoxiaHypoxiaHypoxia-Inducible Factor 1, alpha SubunitPC12 CellsPhenylethyl AlcoholRatsReactive Oxygen SpeciesSignal TransductionTOR Serine-Threonine Kinases3,4-dihydroxyphenylethanolHypoxia-Inducible Factor 1, alpha SubunitmTOR protein, ratPhenylethyl AlcoholPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesTOR Serine-Threonine Kinases

Identifiers

PMID35693707
PMCPMC9187455
OpenAlexW4281777890

What OpenQuestion holds

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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.