ArticleNeural regeneration research2013
JNK3 involvement in nerve cell apoptosis and neurofunctional recovery after traumatic brain injury.
Article in Neural regeneration research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 17 citations in OpenAlex.
- Review
- Novel c-Jun N-Terminal Kinase (JNK) Inhibitors with an 11Molecules (Basel, Switzerland) · 2021Article
- Allograft of Sertoli Cell Transplantation in Combination with Memantine Alleviates Ischemia-Induced Tissue Damages in An Animal Model of Rat.Cell journal · 2020Article
- The Need for SMN-Independent Treatments of Spinal Muscular Atrophy (SMA) to Complement SMN-Enhancing Drugs.Frontiers in neurology · 2020Review
- The Effect of Allograft Transplantation of Sertoli Cell on Expression of NF-кB, Bax Proteins, and Ischemic Tolerance in Rats with Focal Cerebral Ischemia.Iranian journal of pharmaceutical research : IJPR · 2020Article
- 14-3-3ζ protein protects against brain ischemia/reperfusion injury and induces BDNF transcription after MCAO in rat.Journal of applied biomedicine · 2019Article
- Therapeutic Potential of Pretreatment with Allograft Sertoli Cells Transplantation in Brain Ischemia by Improving Oxidative Defenses.Journal of molecular neuroscience : MN · 2018Article
- Neuroprotective effects of pifithrin-α against traumatic brain injury in the striatum through suppression of neuroinflammation, oxidative stress, autophagy, and apoptosis.Scientific reports · 2018Article
- Endoplasmic reticulum stress-induced apoptosis in the penumbra aggravates secondary damage in rats with traumatic brain injury.Neural regeneration research · 2016Article
- Effects of diazepam on glutamatergic synaptic transmission in the hippocampal CA1 area of rats with traumatic brain injury.Neural regeneration research · 2014Article
- AttenuatingBasic and clinical neuroscienceArticle
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence has revealed that the activation of the JNK pathway participates in apoptosis of nerve cells and neurological function recovery after traumatic brain injury. However, which genes in the JNK family are activated and their role in traumatic brain injury remain unclear. Therefore, in this study, in situ end labeling, reverse transcription-PCR and neurological function assessment were adopted to investigate the alteration of JNK1, JNK2 and JNK3 gene expression in cerebral injured rats, and their role in cell apoptosis and neurological function restoration. Results showed that JNK3 expression significantly decreased at 1 and 6 hours and 1 and 7 days post injury, but that JNK1 and JNK2 expression remained unchanged. In addition, the number of apoptotic nerve cells surrounding the injured cerebral cortex gradually reduced over time post injury. The Neurological Severity Scores gradually decreased over 1, 3, 5, 14 and 28 days post injury. These findings suggested that JNK3 expression was downregulated at early stages of brain injury, which may be associated with apoptosis of nerve cells. Downregulation of JNK3 expression may promote the recovery of neurological function following traumatic brain injury.
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