ArticleDrug design, development and therapy2018
Notch inhibitor can attenuate apparent diffusion coefficient and improve neurological function through downregulating NOX2-ROS in severe traumatic brain injury.
Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Astrocytes in functional recovery following central nervous system injuries.The Journal of physiology · 2024Review
- Antidiabetic Drugs Can Reduce the Harmful Impact of Chronic Smoking on Post-Traumatic Brain Injuries.International journal of molecular sciences · 2023Article
- Temporal Expression of Neuroinflammatory and Oxidative Stress Markers and Prostaglandin E2 Receptor EP2 Antagonist Effect in a Rat Model of Epileptogenesis.ACS pharmacology & translational science · 2023Article
- The Notch pathway attenuates burn-induced acute lung injury in rats by repressing reactive oxygen species.Burns & trauma · 2022Article
- Targeting Nrf2-Mediated Oxidative Stress Response in Traumatic Brain Injury: Therapeutic Perspectives of Phytochemicals.Oxidative medicine and cellular longevity · 2022Review
- Self-Sustained Regulation or Self-Perpetuating Dysregulation: ROS-dependent HIF-YAP-Notch Signaling as a Double-Edged Sword on Stem Cell Physiology and Tumorigenesis.Frontiers in cell and developmental biology · 2022Review
- Microenvironmental Variations After Blood-Brain Barrier Breakdown in Traumatic Brain Injury.Frontiers in molecular neuroscience · 2021Review
- Edaravone attenuates smoke inhalation injury in rats by the Notch pathway.American journal of translational research · 2021Article
- An Effective NADPH Oxidase 2 Inhibitor Provides Neuroprotection and Improves Functional Outcomes in Animal Model of Traumatic Brain Injury.Neurochemical research · 2020Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionSecondary brain injury is a major factor that affects the prognosis and outcome of traumatic brain injury (TBI) patients. Secondary brain edema is considered to be an initiating factor in secondary brain injury after TBI. A previous study has indicated that Notch signaling activation contributes to neuron death in mice affected by stroke; however, its role in neuronal oxidation stress for brain edema after TBI is not well established. Apparent diffusion coefficient (ADC) values can represent the brain edema after TBI.
methodsWe established a rat model of acute craniocerebral injury, using functional MRI to evaluate the ADC and cerebral blood flow values. The present study was designed to determine the effect of Notch inhibitor DAPT upon oxidation stress for brain edema after TBI. Rats were randomly distributed into five groups, control group, severe TBI group, severe TBI + vehicle group, severe TBI + DAPT group, and severe TBI + DPI group. All rats were sacrificed at 24 hours after TBI.
resultsOur data indicated that Notch signaling inhibitor DAPT significantly reduced the ADC values and improved the neurological function after TBI. In addition, DAPT decreased NOX2 levels and the ROS levels. Furthermore, DPI can decrease NOX2 levels and ROS levels.
conclusionThis study indicated that DAPT Notch signal inhibitors can inhibit NOX2-ROS generation, reduce the ADC values, relieve cerebral edema, and improve nerve function.
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