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Butin Attenuates Brain Edema in a Rat Model of Intracerebral Hemorrhage by Anti Inflammatory Pathway

BACKGROUND: This study evaluates the effect of butin against brain edema in intracerebral hemorrhage (ICH). METHODOLOGY: ICH was induced by injecting bacterial collagenase in the brain and all the animals were separated into four groups such as control group, ICH group treated with vehicle, Butin 25...

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Detalles Bibliográficos
Autores principales: Li, Peiyu, Jiwu, Cheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: De Gruyter Open 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5941697/
https://www.ncbi.nlm.nih.gov/pubmed/29755784
http://dx.doi.org/10.1515/tnsci-2018-0002
Descripción
Sumario:BACKGROUND: This study evaluates the effect of butin against brain edema in intracerebral hemorrhage (ICH). METHODOLOGY: ICH was induced by injecting bacterial collagenase in the brain and all the animals were separated into four groups such as control group, ICH group treated with vehicle, Butin 25 and 50 mg/kg group receives butin (25 and 50 mg/kg, i.p.)60 min after the induction of ICH in all animals. One day after neurological score, hemorrhagic injury and expressions of protein responsible for apoptosis and inflammatory cytokines were assessed in the brain tissue of ICH rats. RESULT: Neurological scoring significantly increased and hemorrhagic lesion volume decreased in butin treated group of rats compared to ICH group. However, treatment with butin significantly decreases the ratio of Bax/Bcl-2 and protein expression of Cleaved caspase-3 than ICH group in dose dependent manner. Level of inflammatory mediators such as tumor necrosis factor-α (TNF-α) and interlukin-6 (IL-6) in the brain tissues were significantly decreased in the butin treated group than ICH group. In addition butin attenuates the altered signaling pathway of NF-κB in the brain tissues of ICH rats. CONCLUSION: Our study concludes that butin attenuates the altered behavior and neuronal condition in ICH rats by reducing apoptosis and inflammatory response.