ArticleMolecular neurobiology2023
TAT-PEP Alleviated Cognitive Impairment by Alleviating Neuronal Mitochondria Damage and Apoptosis After Cerebral Ischemic Reperfusion Injury.
Article in Molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 8 citations in OpenAlex.
- NMDA Receptor Mediated Mechanisms in the Post-Stroke Brain: From Physiology to Pathology.Biomolecules · 2026Review
- Hydrogen Sulfide Protects Against Cerebral Ischemia-Reperfusion Injury in Rats via S-Sulfhydrating NAMPT to Enhance Mitochondrial Function and Autophagy in Cerebrovascular Endothelial Cells.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Inflammation-centered neurovascular-immune-metabolic remodeling in ischemic stroke: stage-dependent mechanisms, regulated cell death, and therapeutic translation.Frontiers in immunology · 2026Review
- rTMS ameliorates cerebral ischemia-reperfusion injury by inhibiting Golgi apparatus stress through epigenetic modulation of Gli2.Communications biology · 2025Article
- Mitophagy in perioperative neurocognitive disorder: mechanisms and therapeutic strategies.European journal of medical research · 2025Review
- Effect of Fangxia-Dihuang Decoction on doxorubicin-induced cognitive impairment in breast cancer animal model.Frontiers in oncology · 2025Article
- Ginsenoside Rb1 reduced ischemic stroke-induced apoptosis through endoplasmic reticulum stress-associated IRE1/TRAF2/JNK pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Dynamic mechanisms and targeted interventions in cerebral ischemia-reperfusion injury: pathological cascade from ischemia to reperfusion and promising therapeutic strategies.Frontiers in neuroscience · 2025Review
- Exploring Research Trend and Hotspots on Oxidative Stress in Ischemic Stroke (2001-2022): Insights from Bibliometric.Molecular neurobiology · 2024Review
- Advances in understanding the mitochondrial mechanisms underlying acupuncture therapy for post-stroke cognitive impairment.Frontiers in neurologyReview
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Paired immunoglobulin-like receptor B (PirB) was identified as a myelin-associated inhibitory protein (MAIP) receptor that plays a critical role in axonal regeneration, synaptic plasticity and neuronal survival after stroke. In our previous study, a transactivator of transcription-PirB extracellular peptide (TAT-PEP) was generated that can block the interactions between MAIs and PirB. We found that TAT-PEP treatment improved axonal regeneration, CST projection and long-term neurobehavioural recovery after stroke through its effects on PirB-mediated downstream signalling. However, the effect of TAT-PEP on the recovery of cognitive function and the survival of neurons also needs to be investigated. In this study, we investigated whether pirb RNAi could alleviate neuronal injury by inhibiting the expression of PirB following exposure to oxygen-glucose deprivation (OGD) in vitro. In addition, TAT-PEP treatment attenuated the volume of the brain infarct and promoted the recovery of neurobehavioural function and cognitive function. This study also found that TAT-PEP exerts neuroprotection by reducing neuronal degeneration and apoptosis after ischemia-reperfusion injury. In addition, TAT-PEP improved neuron survival and reduced lactate dehydrogenase (LDH) release in vitro. Results also showed that TAT-PEP reduced malondialdehyde (MDA) levels, increased superoxide dismutase (SOD) activity and reduced reactive oxygen species (ROS) accumulation in OGD-injured neurons. The possible mechanism was that TAT-PEP could contribute to the damage of neuronal mitochondria and affect the expression of cleaved caspase 3, Bax and Bcl-2. Our results suggest that PirB overexpression in neurons after ischaemic-reperfusion injury induces neuronal mitochondrial damage, oxidative stress and apoptosis. This study also suggests that TAT-PEP may be a potent neuroprotectant with therapeutic potential for stroke by reducing neuronal oxidative stress, mitochondrial damage, degeneration and apoptosis in ischemic stroke.
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