Evidence map›Paper›PMID 29145851›Full record

ArticleLipids in health and disease2017

ALA/LA ameliorates glucose toxicity on HK-2 cells by attenuating oxidative stress and apoptosis through the ROS/p38/TGF-β

Mingxia Jiang, Haifen Zhang, Lijie Zhai, Bianliang Ye, Yin Cheng, Chengkai Zhai

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Calafate (Antioxidants (Basel, Switzerland) · 2025
    Review
  2. Article
  3. Article
  4. Lipoxin alleviates oxidative stress: a state-of-the-art review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Antioxidants (Basel, Switzerland) · 2020
    Article
  9. Article
  10. Diabetic vasculopathy: macro and microvascular injury.Current pathobiology reports · 2020
    Article
  11. Article
  12. Article
  13. 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

6 authors at 3 institutions in 2 countries.

Mingxia JiangSchool of Public Health, Southeast University, Nanjing, 210009, China.
Haifen ZhangSchool of Public Health, Southeast University, Nanjing, 210009, China.
Lijie ZhaiDepartment of Neurological Surgery, Northwestern University - Feinberg School of Medicine, Chicago, IL, 60612, USA.
Bianliang YeSchool of Public Health, Southeast University, Nanjing, 210009, China.
Yin ChengSchool of Public Health, Southeast University, Nanjing, 210009, China.
Chengkai ZhaiSchool of Public Health, Southeast University, Nanjing, 210009, China. ckzhai@163.com.ORCID http://orcid.org/0000-0001-6366-7273
Southeast University · CNNanjing General Hospital of Nanjing Military Command · CNNorthwestern University · US

Funding

National Natural Science Foundation of China No. 81372986
6 · The paper itself

Abstract

backgroundGrowing evidence indicates that oxidative stress (OS) plays a pivotal role in Diabetic nephropathy (DN). In a previous study we demonstrated that ALA/LA protected HK-2 cells against high glucose-induced cytotoxicity. So we aimed to establish the glucose injury model of HK-2 cells and investigate the beneficial effects of ALA/LA on high glucose-induced excessive production of TGF-β1 and the possible mechanisms mediating the effects.

methodsThe expression of OS markers in high glucose-induced HK-2 cells treated with ALA/LA., including the antioxidant enzymes and reactive oxygen species (ROS) production, as well as the apoptosis rate were assayed by ELISA and flow cytometry. The p38/transforming growth factor β

resultsThe modeling condition of glucose toxicity on HK-2 cells was at the glucose concentration of 40.9 mM. ALA/LA can significantly increase the activities of antioxidant enzymes and decrease ROS production stimulated by high glucose. The study also found that ALA/LA caused a decrease in the apoptosis rate and TGF-β

conclusionsALA/LA exerts protective effects in vitro through inhibition of ROS generation, down regulation of the activation of the p38MAPK pathway and the expression of TGF-β

Indexed as

alpha-Linolenic AcidApoptosisCells, CulturedDiabetic NephropathiesGlucoseHumansLinoleic AcidOxidative StressReactive Oxygen SpeciesSignal TransductionTransforming Growth Factor beta1alpha-Linolenic AcidGlucoseLinoleic AcidReactive Oxygen SpeciesTransforming Growth Factor beta1apoptosisglucose toxicityHK-2 cellslinoleic acid (LA)oxidative stressROS/p38/TGF-β1 pathwayα-linolenic acid (ALA)

Identifiers

PMID29145851
PMCPMC5691398
OpenAlexW2768882109

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.