ArticleNeurobiology of disease2013
PAR-1 antagonist SCH79797 ameliorates apoptosis following surgical brain injury through inhibition of ASK1-JNK in rats.
Article in Neurobiology of disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Protective effect of scutellarin on myocardial cells treated with high glucose.Biomedical reports · 2025Article
- Endothelial Dysfunction in Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Protease-Activated Receptor-1 Antagonist Protects Against Lung Ischemia/Reperfusion Injury.Frontiers in pharmacology · 2021Article
- A Definition of "Multitargeticity": Identifying Potential Multitarget and Selective Ligands Through a Vector Analysis.Frontiers in chemistry · 2020Article
- Surgically-induced brain injury: where are we now?Chinese neurosurgical journal · 2019Review
- Depression following traumatic brain injury in mice is associated with down-regulation of hippocampal astrocyte glutamate transporters by thrombin.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- Thrombin contributes to the injury development and neurological deficit after acute subdural hemorrhage in rats only in collaboration with additional blood-derived factors.BMC neuroscience · 2018Article
- Milk Fat Globule-Epidermal Growth Factor-8 Pretreatment Attenuates Apoptosis and InflammationFrontiers in neurology · 2018Article
- A protease-activated receptor 1 antagonist protects against global cerebral ischemia/reperfusion injury after asphyxial cardiac arrest in rabbits.Neural regeneration research · 2017Article
- Interference with Protease-activated Receptor 1 Alleviates Neuronal Cell Death Induced by Lipopolysaccharide-Stimulated Microglial Cells through the PI3K/Akt Pathway.Scientific reports · 2016Article
- Hydrogen water reduces NSE, IL-6, and TNF-α levels in hypoxic-ischemic encephalopathy.Open medicine (Warsaw, Poland) · 2016Article
- Targeting brain microvascular endothelial cells: a therapeutic approach to neuroprotection against stroke.Neural regeneration research · 2015Review
- Correlation between subacute sensorimotor deficits and brain water content after surgical brain injury in rats.Behavioural brain research · 2015Article
- Contribution of protease-activated receptor 1 in status epilepticus-induced epileptogenesis.Neurobiology of disease · 2015Article
- The protective role of (-)-epigallocatechin-3-gallate in thrombin-induced neuronal cell apoptosis and JNK-MAPK activation.Neuroreport · 2015Article
- Interference with protease-activated receptor 1 does not reduce damage to subventricular zone cells of immature rodent brain following exposure to blood or blood plasma.Journal of negative results in biomedicine · 2015Article
- P2X7R/cryopyrin inflammasome axis inhibition reduces neuroinflammation after SAH.Neurobiology of disease · 2013Article
- CaMKII activates ASK1 to induce apoptosis of spinal astrocytes under oxygen-glucose deprivation.Cellular and molecular neurobiology · 2013Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Neurosurgical procedures inevitably produce intraoperative hemorrhage. The subsequent entry of blood into the brain parenchyma results in the release of large amounts of thrombin, a known contributor to perihematomal edema formation and apoptosis after brain injury. The present study seeks to test 1) the effect of surgically induced brain injury (SBI) on thrombin activity, expression of thrombin's receptor PAR-1, and PAR-1 mediated apoptosis; 2) the effect of thrombin inhibition by argatroban and PAR-1 inhibition by SCH79797 on the development of secondary brain injury in the SBI model on rats. A total of 88 Sprague-Dawley male rats were randomly divided into sham, vehicle-, argatroban-, or SCH79797-treated groups. SBI involved partial resection of the right frontal lobe under inhalation isoflurane anesthesia. Sham-operated animals received only craniotomy. Thrombin activity, brain water content, and neurological deficits were measured at 24 h following SBI. Involvement of the Ask1/JNK pathway in PAR-1-induced post-SBI apoptosis was characterized by using Ask1 or JNK inhibitors. We observed that SBI increased thrombin activity, yet failed to demonstrate any effect on PAR-1 expression. Argatroban and SCH79797 reduced SBI-induced brain edema and neurological deficits in a dose-dependent manner. SBI-induced apoptosis seemed mediated by the PAR-1/Ask1/JNK pathways. Administration of SCH79797 ameliorated the apoptosis following SBI. Our findings indicate that PAR-1 antagonist protects against secondary brain injury after SBI by decreasing both brain edema and apoptosis by inactivating PAR-1/Ask1/JNK pathway. The anti-apoptotic effect of PAR-1 antagonists may provide a promising path for therapy following SBI.
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