ArticleTranslational neuroscience2018
Protective Effects of Epifriedelinol in a Rat Model of Traumatic Brain Injury Assessed with Histological and Hematological Markers.
Article in Translational neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Ferroptosis and mitochondrial dysfunction in acute central nervous system injury.Frontiers in cellular neuroscience · 2023Review
- Blood-Brain Barrier Mechanisms in Stroke and Trauma.Handbook of experimental pharmacology · 2022Review
- Fecal medicines used in traditional medical system of China: a systematic review of their names, original species, traditional uses, and modern investigations.Chinese medicine · 2019Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study evaluated the protective effects of epifriedelinol (EFD) in a rat model of traumatic brain injury (TBI). METHODOLOGY: TBI was induced by dropping a weight from a specific height. The animals were separated into control, TBI, and EFD 100 and 200 mg/kg groups. The latter received 100 and 200 mg/kg EFD, respectively, for 2 days beginning 30 min after inducing TBI. The neurological examination score, permeability of the blood-brain barrier (BBB), water content of the brain, cytokine levels, and oxidative stress parameters were measured in the rats. The effects of EFD on glial fibrillary acidic protein (GFAP)-positive cells were evaluated using immunohistochemistry.
resultThe EFD treatment significantly decreased the neurological score, permeability of the BBB, and water content of brain compared with the TBI group. The levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and oxidative stress were significantly decreased in the EFD-treated groups. The number of GFAP-positive cells was also significantly reduced in the EFD-treated groups.
conclusionEFD attenuates the secondary injury in TBI rats by reducing the serum cytokine levels and oxidative stress.
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Registered trials
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