Evidence map›Paper›PMID 25684163›Full record

ArticleMolecular medicine reports2015

α-Lipoic acid protects against hypoxia/reoxygenation-induced injury in human umbilical vein endothelial cells through suppression of apoptosis and autophagy.

Jingjing Zhang, Houliang Deng, Li Liu, Xiaoxia Liu, Xialin Zuo, Qian Xu, Zhuomin Wu, Xiaobin Peng, Aimin Ji

Abstract read
In one paragraph

Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Sitagliptin attenuates endothelial dysfunction independent of its blood glucose controlling effect.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
    Article
  4. Article
  5. Article
  6. Article
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

9 authors.

Jingjing ZhangCenter for Drug Research and Development, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
Houliang DengCenter for Drug Research and Development, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
Li LiuCenter for Drug Research and Development, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
Xiaoxia LiuCenter for Drug Research and Development, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
Xialin ZuoInstitute of Neurosciences, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510260, P.R. China.
Qian XuCenter for Drug Research and Development, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
Zhuomin WuCenter for Drug Research and Development, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.
Xiaobin PengSchool of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Aimin JiCenter for Drug Research and Development, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

α-Lipoic acid (ALA) is known as a powerful antioxidant, which has been reported to have protective effects against various cardiovascular diseases. The present study aimed to determine whether ALA pre- or post-treatment induced protective effects against hypoxia/reoxygenation-induced injury via inhibition of apoptosis and autophagy in human umbilical vein endothelial cells (HUVECs). In order to simulate the conditions of hypoxia/reoxygenation, HUVECs were subjected to 4 h of oxygen-glucose deprivation (OGD) followed by 12 h of reoxygenation. For the pre-treatment, ALA was added to the buffer 12 h prior to OGD, whereas for the post-treatment, ALA was added at the initiation of reoxygenation. The results demonstrated that ALA pre- or post-treatment significantly reduced lactate dehydrogenase (LDH) release induced through hypoxia/reoxygenation in HUVECs in a dose-dependent manner; of note, 1 mM ALA pre- or post-treatment exhibited the most potent protective effects. In addition, ALA significantly reduced hypoxia/reoxygenation-induced loss of mitochondrial membrane potential, apoptosis and the expression of cleaved caspase-3 in HUVECs. In the presence of the specific autophagy inhibitor 3-methyladenine, hypoxia/reoxygenation-induced apoptosis was significantly reduced. Furthermore, the formation of autophagosomes, cytosolic microtubule-associated protein 1A/1B-light chain 3 ratio and beclin1 levels significantly increased following hypoxia/reoxygenation injury; however, all of these effects were ameliorated following pre- or post-treatment with ALA. The results of the present study suggested that ALA may provide beneficial protection against hypoxia/reoxygenation-induced injury via attenuation of apoptosis and autophagy in HUVECs.

Indexed as

AdenineAntioxidantsApoptosisApoptosis Regulatory ProteinsAutophagyBeclin-1Caspase 3Cell HypoxiaDose-Response Relationship, DrugGene ExpressionGlucoseHumansHuman Umbilical Vein Endothelial CellsL-Lactate DehydrogenaseMembrane Potential, MitochondrialMembrane Proteins3-methyladenineAdenineAntioxidantsApoptosis Regulatory ProteinsBeclin-1BECN1 protein, humanCaspase 3GlucoseL-Lactate DehydrogenaseMembrane ProteinsMicrotubule-Associated ProteinsOxygenThioctic Acid

Identifiers

PMID25684163
PMCPMC4438966

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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.