ArticlePPAR research2014
Decrease of PPARδ in Type-1-Like Diabetic Rat for Higher Mortality after Spinal Cord Injury.
Article in PPAR research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Role of PPAR-β/δ/miR-17/TXNIP pathway in neuronal apoptosis after neonatal hypoxic-ischemic injury in rats.Neuropharmacology · 2018Article
- Critical role of mTOR, PPARγ and PPARδ signaling in regulating early pregnancy decidual function, embryo viability and feto-placental growth.Molecular human reproduction · 2018Article
- Identification of key genes and pathways associated with spinal cord injury.Molecular medicine reports · 2017Article
- PPARδ agonist GW0742 ameliorates Aβ1-42-induced hippocampal neurotoxicity in mice.Metabolic brain disease · 2016Article
- Hippocampal PPARδ Overexpression or Activation Represses Stress-Induced Depressive Behaviors and Enhances Neurogenesis.The international journal of neuropsychopharmacology · 2015Article
- RNA-seq identifies a role for the PPARβ/δ inverse agonist GSK0660 in the regulation of TNFα-induced cytokine signaling in retinal endothelial cells.Molecular vision · 2015Article
- Development of telmisartan in the therapy of spinal cord injury: pre-clinical study in rats.Drug design, development and therapy · 2015Article
Corrections and comments
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Authors and funding
6 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes in the peroxisome proliferator-activated receptors- δ (PPAR δ ) expression in rats after spinal cord injury (SCI) have been previously reported. Diabetic animals show a higher mortality after SCI. However, the relationship between the progress of diabetes and PPAR δ in SCI remains unknown. In the present study, we used compressive SCI in streptozotocin-(STZ-) induced diabetic rats. GW0742, a PPAR δ agonist, was used to evaluate its merit in STZ rats after SCI. Changes in PPAR δ expression were detected by Western blot. Survival rates were also estimated. A lower expression of PPAR δ in spinal cords of STZ-diabetic rats was observed. In addition, the survival times in two-week induction diabetes were longer than those in eight-week induction group, which is consistent with the expression of PPAR δ in the spinal cord. Moreover, GW0742 significantly increased the survival time of STZ rats. Furthermore, their motor function and pain response were attenuated by GSK0660, a selective PPAR δ antagonist, but were enhanced by GW0742. In conclusion, the data suggest that higher mortality rate in STZ-diabetic rats with SCI is associated with the decrease of PPAR δ expression. Thus, change of PPAR δ expression with the progress of diabetes seems responsible for the higher mortality rate after SCI.
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Registered trials
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