ArticleExperimental and therapeutic medicine2020
Imatinib inhibits oxidative stress response in spinal cord injury rats by activating Nrf2/HO-1 signaling pathway.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.
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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
13 citing papers in PubMed, 29 citations in OpenAlex.
- Imatinib prevents blood-spinal cord barrier disruption by inhibiting PDGFR-mediated JMJD3 expression and activation after spinal cord injury.Fluids and barriers of the CNS · 2025Article
- Nrf2 Signaling Pathway: Focus on Oxidative Stress in Spinal Cord Injury.Molecular neurobiology · 2025Review
- The protective effect of imatinib against pancreatic β-cell apoptosis induced by dexamethasone via increased GSTP1 expression and reduced oxidative stress.Scientific reports · 2024Article
- Effects of lercanidipine on traumatic spinal cord injury: an experimental study.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2024Article
- Advancements in neuroregenerative and neuroprotective therapies for traumatic spinal cord injury.Frontiers in neuroscience · 2024Review
- ROS: Executioner of regulating cell death in spinal cord injury.Frontiers in immunology · 2024Review
- Pharmacological interventions targeting the microcirculation following traumatic spinal cord injury.Neural regeneration research · 2024Review
- Blood-spinal cord barrier disruption in degenerative cervical myelopathy.Fluids and barriers of the CNS · 2023Review
- Article
- The mechanism by which hyperbaric oxygen treatment alleviates spinal cord injury: genome-wide transcriptome analysis.Neural regeneration research · 2022Article
- Imatinib inhibits pericyte-fibroblast transition and inflammation and promotes axon regeneration by blocking the PDGF-BB/PDGFRβ pathway in spinal cord injury.Inflammation and regeneration · 2022Article
- Recent Advances in the Role of Nuclear Factor Erythroid-2-Related Factor 2 in Spinal Cord Injury: Regulatory Mechanisms and Therapeutic Options.Frontiers in aging neuroscience · 2022Review
- Role of ABT888, a Novel Poly(ADP-Ribose) Polymerase (PARP) Inhibitor in Countering Autophagy and Apoptotic Processes Associated to Spinal Cord Injury.Molecular neurobiology · 2020Article
Corrections and comments
- Retraction · 2023-10-30Concerns/Issues about Data · Duplication of/in Image · Error in Methods · Euphemisms for Duplication · Investigation by Journal/Publisher · Investigation by Third Party · Paper Mill · Results Not Reproducible · Unreliable Data · · seee also: https://pubpeer.com/publications/A611A2FDDDB179FC736FD864020BEE
- Retracted
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Effect of imatinib on rats with spinal cord injury (SCI) was investigated through the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. Forty-eight Sprague-Dawley rats were randomly divided into sham operation group (n=12), model group (n=12), imatinib group (n=12) and inhibitor group (n=12). The results of immunohistochemistry showed that in comparison with sham operation group, the other three groups had overtly increased positive expression level of Bax and evidently reduced positive expression level of Bcl-2 (P<0.05). Compared with those in model group and inhibitor group, the positive expression level of Bax was distinctly lower, while that of Bcl-2 was notably increased in imatinib group (P<0.05). According to western blot analysis, the protein expression levels of Nrf2 and HO-1 were obviously higher in the other three groups than those in sham operation group (P<0.05), and they were remarkably higher in imatinib group than those in model group and inhibitor group (P<0.05). The results of qPCR assay revealed that the Nrf2 and HO-1 mRNA expression levels were markedly elevated in the other three groups compared with those in sham operation group (P<0.05). Based on ELISA, the other three groups exhibited notably raised content of IL-6, TNF-α, ROS and SOD compared with sham operation group (P<0.05), and imatinib group displayed remarkably decreased content of IL-6, TNF-α and ROS and markedly elevated SOD content in comparison with model group and inhibitor group (P<0.05). The results of TUNEL assay demonstrated that the rate of apoptosis was significantly raised in the other three groups compared with that in sham operation group (P<0.05), and it declined obviously in imatinib group compared with that in model group and inhibitor group (P<0.05). Imatinib inhibits oxidative stress response in SCI rats by activating the Nrf2/HO-1 signaling pathway, thus repressing apoptosis and inflammation.
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