Evidence map›Paper›PMID 30587838›Full record

ArticleMolecules (Basel, Switzerland)2018

Gigantol has Protective Effects against High Glucose-Evoked Nephrotoxicity in Mouse Glomerulus Mesangial Cells by Suppressing ROS/MAPK/NF-κB Signaling Pathways.

Mei-Fen Chen, Shorong-Shii Liou, Tang-Yao Hong, Shung-Te Kao, I-Min Liu

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Chemical Constituents and Hypoglycemic Mechanisms ofMolecules (Basel, Switzerland) · 2023
    Article
  4. Review
  5. International journal of molecular sciences · 2022
    Article
  6. [Exploring the therapeutic mechanism ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. p38/TF/HIF-BioMed research international · 2019
    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

5 authors at 2 institutions in 1 country.

Mei-Fen ChenSchool of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung 40402, Taiwan. chen0922265113@gmail.com.
Shorong-Shii LiouDepartment of Pharmacy and Master Program, Collage of Pharmacy and Health Care, Tajen University, Pingtung County 90741, Taiwan. ssliou@tajen.edu.tw.
Tang-Yao HongDepartment of Biotechnology, Collage of Pharmacy and Health Care, Tajen University, Pingtung County 90741, Taiwan. tyhong@tajen.edu.tw.
Shung-Te KaoSchool of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung 40402, Taiwan. stkao@mail.cmu.edu.tw.
I-Min LiuDepartment of Pharmacy and Master Program, Collage of Pharmacy and Health Care, Tajen University, Pingtung County 90741, Taiwan. iml@tajen.edu.tw.
Tajen University · TWChina Medical University · TW

Funding

Ministry of Science and Technology, Taiwan MOST 107-2320-B-127-001
6 · The paper itself

Abstract

Gigantol is a bibenzyl compound derived from several medicinal orchids. This biologically active compound has shown promising therapeutic potential against diabetic cataracts, but whether this compound exerts beneficial effects on the other diabetic microvascular complications remains unclear. This study was carried out to examine effects of gigantol on high glucose-induced renal cell injury in cultured mouse kidney mesangial cells (MES-13). MES-13 cells were pretreated with gigantol (1, 5, 10 or 20 μmol/L) for 1 h followed by further exposure to high (33.3 mmol/L) glucose for 48 h. Gigantol concentration dependently enhanced cell viability followed by high glucose treatment in MES-13 cells. High glucose induced reactive oxygen species (ROS) generation, malondialdehyde production and glutathione deficiency were recoved in MES-13 cells pretreated with gigantol. High glucose triggered cell apoptosis via the the loss of mitochondrial membrane potential, depletion of adenosine triphosphate, upregulation of caspases 9 and 3, enhancement of cytochrome c release, and subsequent interruption of the Bax/Bcl-2 balance. These detrimental effects were ameliorated by gigantol. High glucose also induced activation of JNK, p38 mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) in MES-13 cells, which were blocked by gigantol. The results suggest that treatment MES-13 cells with gigantol halts high glucose-induced renal dysfunction through the suppression of the ROS/MAPK/NF-κB signaling pathways. Our data are of value to the understanding the mechanism for gigantol, and would benefit the study of drug development or food supplement for diabetes and nephropathy.

Indexed as

AnimalsApoptosisBibenzylsCell LineCells, CulturedCell SurvivalDiabetic NephropathiesGlucoseGuaiacolLipid PeroxidationMesangial CellsMiceMitochondriaMitogen-Activated Protein KinasesNF-kappa BOxidative StressBibenzylsgigantolGlucoseGuaiacolMitogen-Activated Protein KinasesNF-kappa BProtective AgentsReactive Oxygen Speciesdiabetic nephropathygigantolhigh glucoseMES-13 cellsmitogen-activated protein kinaseNF-κB

Identifiers

PMID30587838
PMCPMC6337535
OpenAlexW2906085175

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.