ReferenceID 5410
miR-23b/TAB3/NF-κB/p53 axis is involved in hippocampus injury induced by cerebral ischemia-reperfusion in rats: The protective effect of chlorogenic acid
Biofactors
Apoptosis is the main pathological aspect of neuronal injury after cerebral ischemia-reperfusion (I/R) injury. However the detailed molecular mediators are still under debate. The aim of this study is to explore the effe
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Record Fields
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- Reference Id
- 5410
- Evidence Id
- 22000
- Core Evidence Id
- 22000
- Source Reference Id
- 4079
- Herb2 Reference Id
- HBREF004876
- Subject Paper Key
- HBIN029163_35201648
- Pubmed Id
- 35201648
- Doi
- 10.1002/biof.1830
- Paper Title
- miR-23b/TAB3/NF-κB/p53 axis is involved in hippocampus injury induced by cerebral ischemia-reperfusion in rats: The protective effect of chlorogenic acid
- Paper Abstract
- Apoptosis is the main pathological aspect of neuronal injury after cerebral ischemia-reperfusion (I/R) injury. However the detailed molecular mediators are still under debate. The aim of this study is to explore the effect of cerebral I/R on miR-23a/TGF-β-activated kinase 1 binding protein 3 (TAB3)/nuclear factor kappa B (NF-κB)/p53 axis in rat hippocampus alone and in combination with chlorogenic acid (CGA). Common carotid artery occlusion (CCAO) was performed by nylon monofilament for 20 min to establish a model of ischemic brain injury. CGA (30 mg/kg) was administered intraperitoneally (ip), 10 min prior to ischemia and 10 min before reperfusion. Examination of hippocampus neurons by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining showed that the number of apoptotic neurons was elevated at 24 h after reperfusion. At the molecular levels, I/R injury resulted in an increased protein expression of p53 with a concomitant upregulation of cleaved-caspase3/phosphorelated-caspase3 ratio and cytochrome c level. Further miR-23b gene expression was significantly downregulated after 24 h of reperfusion. Also, we observed increased TAB3 and NF-κB protein expressions after 24 h following CCAO. Treatment with CGA significantly reduced the apoptotic damage and also reversed miR-23b gene expression, TAB3 and NF-κB protein expressions in hippocampus neurons in I/R rats. In conclusion our data suggest that miR-23b/TAB3/NF-κB/p53 axis could play a regulatory role in hippocampus cell death, which provide a new target for novel therapeutic interventions during transit ischemic stroke. It also demonstrated that CGA could reverse these molecular alterations indicating an effective component against hippocampus apoptotic insult following acute I/R injury.
- Journal
- Biofactors
- Publish Year
- 2022
- Experiment Subject
- rat
- Experiment Type
- Animal Experiment
- Phenotype Related
- Cerebral Ischemia-reperfusion (i/r) Injury; Ischemic Brain Injury; Carotid Artery Occlusion; Neuronal Injury; Acute I/r Injury; Ischemic Stroke
- Paper Title Cn
- Paper Title En
- miR-23b/TAB3/NF-κB/p53 axis is involved in hippocampus injury induced by cerebral ischemia-reperfusion in rats: The protective effect of chlorogenic acid
- Bilingual Status
- semi_complete