Peri-Injury Stearidonic Acid Ethanolamide Modulates Astroglial Reactivity-Associated Markers in a Mouse Model of Mild Traumatic Brain Injury.
- 1A.V. Zhirmunsky National Scientific Center of Marine Biology, Far Eastern Branch, Russian Academy of Sciences, Vladivostok 690041, Russia.
Abstract
Background/objectives
Mild traumatic brain injury (mTBI) can cause persistent neuroinflammation and astroglial reactivity. This study examined whether peri-injury administration of stearidonic acid ethanolamide (SDEA) was associated with changes in astrocyte-associated responses after mTBI and in primary astroglial cultures.Methods
Male C57BL/6 mice received SDEA (10 mg/kg, subcutaneously) for 2 days before mTBI, immediately after injury, and for 7 days thereafter. At 11 weeks post-injury, cortical GFAP immunoreactivity and the expression of astrocyte-associated markers, PPAR isoforms, and neurotrophic factors were assessed by immunohistochemistry and RT-qPCR. Primary astroglial cultures were treated with 1 or 10 μM SDEA for 48 h.Results
SDEA attenuated mTBI-associated increases in GFAP-positive cells and cortical Gfap and C3 expression while increasing S100a10 and Clcf1 expression. SDEA treatment was accompanied by increased cortical Ppara and Pparg mRNA expression and changes in the expression of neurotrophic-factor genes. In cultured astroglia, SDEA increased S100a10, Clcf1, Ppara, Pparg, Bdnf, Ngf, and Gdnf mRNA expression without significantly altering Gfap or C3.Conclusions
Peri-injury SDEA administration was associated with reduced chronic cortical GFAP reactivity and changes in selected astrocyte-associated transcripts after mTBI.
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BibTeX
@article{girich2026periinjury,
title = {{Peri-Injury Stearidonic Acid Ethanolamide Modulates Astroglial Reactivity-Associated Markers in a Mouse Model of Mild Traumatic Brain Injury.}},
author = {Anastasia Girich and Igor Manzhulo and Darya Ivashkevich and Arina Ponomarenko and Anna Tyrtyshnaia},
journal = {Pathophysiology : the official journal of the International Society for Pathophysiology},
year = {2026},
month = oct,
doi = {10.3390/pathophysiology33040078},
url = {https://europepmc.org/article/MED/42924829},
note = {CC BY},
}
RIS
TY - JOUR
TI - Peri-Injury Stearidonic Acid Ethanolamide Modulates Astroglial Reactivity-Associated Markers in a Mouse Model of Mild Traumatic Brain Injury.
AU - Anastasia Girich
AU - Igor Manzhulo
AU - Darya Ivashkevich
AU - Arina Ponomarenko
AU - Anna Tyrtyshnaia
PY - 2026
DA - 2026/10/20
JO - Pathophysiology : the official journal of the International Society for Pathophysiology
DO - 10.3390/pathophysiology33040078
UR - https://europepmc.org/article/MED/42924829
AB - Background/objectives Mild traumatic brain injury (mTBI) can cause persistent neuroinflammation and astroglial reactivity. This study examined whether peri-injury administration of stearidonic acid ethanolamide (SDEA) was associated with changes in astrocyte-associated responses after mTBI and in primary astroglial cultures.Methods Male C57BL/6 mice received SDEA (10 mg/kg, subcutaneously) for 2 days before mTBI, immediately after injury, and for 7 days thereafter. At 11 weeks post-injury, cortical GFAP immunoreactivity and the expression of astrocyte-associated markers, PPAR isoforms, and neurotrophic factors were assessed by immunohistochemistry and RT-qPCR. Primary astroglial cultures were treated with 1 or 10 μM SDEA for 48 h.Results SDEA attenuated mTBI-associated increases in GFAP-positive cells and cortical Gfap and C3 expression while increasing S100a10 and Clcf1 expression. SDEA treatment was accompanied by increased cortical Ppara and Pparg mRNA expression and changes in the expression of neurotrophic-factor genes. In cultured astroglia, SDEA increased S100a10, Clcf1, Ppara, Pparg, Bdnf, Ngf, and Gdnf mRNA expression without significantly altering Gfap or C3.Conclusions Peri-injury SDEA administration was associated with reduced chronic cortical GFAP reactivity and changes in selected astrocyte-associated transcripts after mTBI.
SN - 0928-4680
SN - 1873-149X
ER -