Evidence map›Paper›PMID 30796627›Full record

ArticleJournal of physiology and biochemistry2019

Protective effects of atorvastatin on high glucose-induced oxidative stress and mitochondrial apoptotic signaling pathways in cultured chondrocytes.

Azam Hosseinzadeh, Kobra Bahrampour Juybari, Tunku Kamarul, Ali Mohammad Sharifi

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of physiology and biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. [Research Progress in Glucose Metabolism of Chondrocytes].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021
    Review
  15. Article
  16. Effects of statins on mitochondrial pathways.Journal of cachexia, sarcopenia and muscle · 2021
    Review
  17. 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

4 authors at 3 institutions in 2 countries.

Azam HosseinzadehRazi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran.
Kobra Bahrampour JuybariDepartment of Pharmacology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran.
Tunku KamarulTissue Engineering Group, (NOCERAL), Department of Orthopedics Surgery, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
Ali Mohammad SharifiRazi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran. sharifalim@gmail.com.ORCID http://orcid.org/0000-0002-5089-7122
Iran University of Medical Sciences · IRSemnan University of Medical Sciences · IRUniversity of Malaya · MY

Funding

Iran Univeristy of Medical Sciences 29686
6 · The paper itself

Abstract

The high glucose concentration is able to disturb chondrocyte homeostasis and contribute to OA pathogenesis. This study was designed to investigate the protective effects of atorvastatin (ATO) on high glucose (HG)-mediated oxidative stress and mitochondrial apoptosis in C28I2 human chondrocytes. The protective effect of ATO (0.01 and 0.1 μM) on HG (75 mM)-induced oxidative stress and apoptosis was evaluated in C28I2 cells. The effects of ATO on HG-induced intracellular ROS production and lipid peroxidation were detected and the protein expression levels of Bax, Bcl-2, caspase-3, total and phosphorylated JNK and P38 MAPKs were analyzed by Western blotting. The mRNA expression levels of antioxidant enzymes including heme oxygenase-1, NAD(P)H quinine oxidoreductase, glutathione S-transferase-P1, catalase, superoxide dismutase-1, glutathione peroxidase-1, -3, -4 were evaluated by reverse transcription-polymerase chain reaction. Pretreatment with ATO remarkably increased the gene expression levels of antioxidant enzymes and reduced HG-induced elevation of ROS, lipid peroxidation, Bax/Bcl-2 ratio, caspase-3 activation, and JNK and P38 phosphorylation. Atorvastatin could considerably reduce HG-induced oxidative stress and mitochondrial apoptosis through increasing the expression of antioxidant enzymes. Atorvastatin may be considered as a promising agent to prevent high glucose-induced cartilage degradation in OA patients.

Indexed as

ApoptosisAtorvastatinbcl-2-Associated X ProteinCaspase 3Cell LineChondrocytesGlucoseHumansLipid PeroxidationMAP Kinase Kinase 4MitochondriaOxidative StressOxidoreductasesp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesAtorvastatinbcl-2-Associated X ProteinBCL2 protein, humanCASP3 protein, humanCaspase 3GlucoseMAP Kinase Kinase 4Oxidoreductasesp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesApoptosisAtorvastatinHigh glucoseOsteoarthritisReactive oxygen species

Identifiers

PMID30796627
OpenAlexW2915510829

What OpenQuestion holds

Textmetadata
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.