ArticleBasic and clinical neuroscience
Hippocampal Astrocyte Response to Melatonin Following Neural Damage Induction in Rats.
Article in Basic and clinical neuroscience. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- Melatonin Modulates Astrocyte Inflammatory Response and Nrf2/SIRT1 Signaling Pathways in Adult Rat Cortical Cultures.Biomedicines · 2025Article
- Reaction of different cell types of the brain on neurotoxin cuprizone and hormone melatonin treatment in young and aging mice.Frontiers in cellular neuroscience · 2023Article
- Melatonin as the Cornerstone of Neuroimmunoendocrinology.International journal of molecular sciences · 2022Review
- The role of circadian clock in astrocytes: From cellular functions to ischemic stroke therapeutic targets.Frontiers in neuroscience · 2022Review
Corrections and comments
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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
introductionBrain injury induces an almost immediate response from glial cells, especially astrocytes. Activation of astrocytes leads to the production of inflammatory cytokines and reactive oxygen species that may result in secondary neuronal damage. Melatonin is an anti-inflammatory and antioxidant agent, and it has been reported to exert neuroprotection through the prevention of neuronal death in several models of central nervous system injury. This study aimed to investigate the effect of melatonin on astrocyte activation induced by Traumatic Brain Injury (TBI) in rat hippocampus and dentate gyrus.
methodsAnimals were randomly divided into 5 groups; Sham group, TBI group, vehicle group, and melatonin-treated TBI groups (TBI+Mel5, TBI+Mel20). Immunohistochemical method (GFAP marker) and TUNEL assay were used to evaluate astrocyte reactivity and neuronal death, respectively.
resultsThe results demonstrated that the astrocyte number was reduced significantly in melatonin-treated groups compared to the vehicle group. Additionally, based on TUNEL results, melatonin administration noticeably reduced the number of apoptotic neurons in the rat hippocampus and dentate gyrus.
conclusionIn general, our findings suggest that melatonin treatment after brain injury reduces astrocyte reactivity as well as neuronal cell apoptosis in rat hippocampus and dentate gyrus.
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