ArticleJournal of molecular neuroscience : MN2018
Neuregulin-1β Plays a Neuroprotective Role by Inhibiting the Cdk5 Signaling Pathway after Cerebral Ischemia-Reperfusion Injury in Rats.
Article in Journal of molecular neuroscience : MN, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- Nrg1 regulates cortical wiring and motor recovery upon traumatic injury.Frontiers in cellular neuroscience · 2026Article
- Cyclin-dependent kinases (CDKs) are key genes regulating early development of Neptunea arthritica cumingii: evidence from comparative transcriptome and proteome analyses.BMC genomics · 2024Article
- HIF-1α knockdown attenuates inflammation and oxidative stress in ischemic stroke male rats via CXCR4/NF-κB pathway.Brain and behavior · 2024Article
- HSP90β regulates EAAT2 expression and participates in ischemia‑reperfusion injury in rats.Molecular medicine reports · 2024Article
- Network Pharmacology Analysis and Experimental Validation of Kaempferol in the Treatment of Ischemic Stroke by Inhibiting Apoptosis and Regulating Neuroinflammation Involving Neutrophils.International journal of molecular sciences · 2022Article
- Article
- The role of Cdk5 in neurological disorders.Frontiers in cellular neuroscience · 2022Review
- Neuregulin-1 alleviate oxidative stress and mitigate inflammation by suppressing NOX4 and NLRP3/caspase-1 in myocardial ischaemia-reperfusion injury.Journal of cellular and molecular medicine · 2021Article
- Review
- The Cerebroprotein Hydrolysate-I Plays a Neuroprotective Effect on Cerebral Ischemic Stroke by Inhibiting MEK/ERK1/2 Signaling Pathway in Rats.Neuropsychiatric disease and treatment · 2021Article
- Effects of Thymoquinone on Small-Molecule Metabolites in a Rat Model of Cerebral Ischemia Reperfusion Injury Assessed using MALDI-MSI.Metabolites · 2020Article
- Hederagenin Attenuates Cerebral Ischaemia/Reperfusion Injury by Regulating MLK3 Signalling.Frontiers in pharmacology · 2020Article
- NMDA Receptors Regulate Neuregulin 2 Binding to ER-PM Junctions and Ectodomain Release by ADAM10 [corrected].Molecular neurobiology · 2019Article
- CDK5: Key Regulator of Apoptosis and Cell Survival.Biomedicines · 2019Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
This study investigated the effects of neuregulin-1β (NRG1β) after middle cerebral artery occlusion/reperfusion (MCAO/R) in rats to evaluate whether they occur via the cyclin-dependent kinase (Cdk)5 signaling pathway. One hundred adult male Wistar rats were randomly divided into sham, MCAO/R, treatment (NRG1β), inhibitor (roscovitine; Ros), and inhibitor + treatment (Ros + NRG1β) groups. The MCAO/R model was established using the intraluminal thread method. The neurobehavioral function was evaluated by the modified neurological severity score (mNSS). The cerebral infarction volume (CIV) was measured by triphenyl tetrazolium chloride (TTC) staining. Morphological changes were observed by hematoxylin-eosin (HE) staining. The apoptotic cell index (ACI) was detected by the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. Immunohistochemistry and Western blotting were performed to detect the expression of calpain 1, p35/p25 (regulatory binding partners of Cdk5), Cdk5, and p-Tau in neurons. The neuronal morphology in the MCAO/R, NRG1β, Ros + NRG1β, and Ros groups differed compared to the sham group; the mNSS, CIV, ACI, and the expression of calpain 1, p35/p25, Cdk5, and p-Tau were significantly increased in all four groups (P < 0.05). In the NRG1β, Ros and Ros + NRG1β groups, the neuronal morphology was significantly improved compared to the MCAO/R group, as were the mNSS, CIV, and ACI. The levels of calpain 1, p35/p25, and p-Tau were decreased compared with the MCAO/R group (P < 0.05), while the Cdk5 expression was not significantly different (P > 0.05). NRG1β may exert neuroprotective effects by inhibiting the expression of calpain 1, p35/p25, and p-Tau after cerebral ischemia-reperfusion injury.
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