ArticleFrontiers in neuroscience2019
2-BFI Provides Neuroprotection Against Inflammation and Necroptosis in a Rat Model of Traumatic Brain Injury.
Article in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Therapeutic Potential of 2-(2-Benzofuranyl)-2-Imidazoline in Preclinical CNS Models: A Systematic Review of Mechanisms, Disease Models, and Cellular Targets.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Review
- Expression of RIPK-1 and S-100B in traumatic brain injury- exploring a forensic cases series.International journal of legal medicine · 2025Article
- Intricate Role of the Cyclic Guanosine Monophosphate Adenosine Monophosphate Synthase-Stimulator of Interferon Genes (cGAS-STING) Pathway in Traumatic Brain Injury-Generated Neuroinflammation and Neuronal Death.ACS pharmacology & translational science · 2024Review
- RACK1 promotes autophagy via the PERK signaling pathway to protect against traumatic brain injury in rats.CNS neuroscience & therapeutics · 2024Article
- An overview of preclinical models of traumatic brain injury (TBI): relevance to pathophysiological mechanisms.Frontiers in cellular neuroscience · 2024Review
- Inhibition of the RIP3/MLKL/TRPM7 necroptotic pathway ameliorates diabetes mellitus-induced erectile dysfunction by reducing cell death, fibrosis, and inflammation.Frontiers in pharmacology · 2024Article
- Role of necroptosis in traumatic brain and spinal cord injuries.Journal of advanced research · 2022Review
- The role of regulatory necrosis in traumatic brain injury.Frontiers in molecular neuroscience · 2022Review
- The Key Regulator of Necroptosis, RIP1 Kinase, Contributes to the Formation of Astrogliosis and Glial Scar in Ischemic Stroke.Translational stroke research · 2021Article
- Article
- 2-(2-Benzofuranyl)-2-Imidazoline Attenuates the Disruption of the Blood-Brain Barrier in EAE via NMDAR.Neurochemical research · 2021Article
- Controlled Decompression Attenuates Compressive Injury following Traumatic Brain Injury via TREK-1-Mediated Inhibition of Necroptosis and Neuroinflammation.Oxidative medicine and cellular longevity · 2021Article
- Necroptosis: A Novel Pathway in Neuroinflammation.Frontiers in pharmacology · 2021Review
- Nrf2/HO-1 mediates the neuroprotective effects of pramipexole by attenuating oxidative damage and mitochondrial perturbation after traumatic brain injury in rats.Disease models & mechanisms · 2020Article
- Arc silence aggravates traumatic neuronal injury via mGluR1-mediated ER stress and necroptosis.Cell death & disease · 2020Article
- Combined Treatment With 2-(2-Benzofu-Ranyl)-2-Imidazoline and Recombinant Tissue Plasminogen Activator Protects Blood-Brain Barrier Integrity in a Rat Model of Embolic Middle Cerebral Artery Occlusion.Frontiers in pharmacology · 2020Article
- Recombinant CC16 inhibits NLRP3/caspase-1-induced pyroptosis through p38 MAPK and ERK signaling pathways in the brain of a neonatal rat model with sepsis.Journal of neuroinflammation · 2019Article
- Silencing of A20 Aggravates Neuronal Death and Inflammation After Traumatic Brain Injury: A Potential Trigger of Necroptosis.Frontiers in molecular neuroscience · 2019Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation and programmed necrosis (necroptosis) are the two hallmark pathological changes after traumatic brain injury (TBI) that contribute to aggravated brain damage. 2-(2-Benzofuranyl)-2-imidazoline (2-BFI) has been shown to exert both anti-inflammatory and programmed cell death effects. Therefore, the aim of the present study was to evaluate the potential beneficial effects of 2-BFI in a rat model of TBI induced by a weight-drop device. 2-BFI or vehicle was given via intraperitoneal injection starting at 30 min post trauma and then twice daily for three consecutive days. Following a neurofunctional test at 72 h after injury, histological, molecular, and immunohistochemistry analyses were performed on the pericontusional areas of the brain. 2-BFI treatment significantly attenuated neurological deficits, brain edema and blood-brain barrier permeability after TBI. Also, treatment with 2-BFI significantly reduced microglial activation, neutrophil infiltration, and proinflammatory cytokine interleukin (IL)-1β secretion, which is related to nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation after TBI. In addition, 2-BFI treatment markedly reduced cortical tissue loss as well as repressed TBI-induced increases in necroptosis and necroptosis-associated proteins, including receptor-interacting protein (RIP1), RIP3, and mixed linkage kinase domain-like (MLKL) in the pericontusional brain tissue. Taken together, these findings indicate that 2-BFI may be an effective neuroprotectant after brain trauma and warrants further study.
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