Peri-Injury Stearidonic Acid Ethanolamide Modulates Astroglial Reactivity-Associated Markers in a Mouse Model of Mild Traumatic Brain Injury

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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.