AI Article Synopsis
- - The study investigates the protective effects of Growth arrest-specific gene 6 (Gas6) against cognitive and emotional impairments in sepsis survivors, specifically focusing on sepsis-associated encephalopathy (SAE).
- - Researchers induced sepsis in mice and then administered Gas6, finding that it significantly improved neurological functions and reduced brain swelling and blood-brain barrier (BBB) damage.
- - The results indicate that Gas6 could potentially help reverse neurological deficits and protect against SAE by restoring BBB integrity and increasing the expression of critical tight junction proteins.
Article Abstract
Objective: Sepsis-associated encephalopathy (SAE), characterized by cognitive and emotional impairments, is not well investigated in sepsis survivors. Growth arrest-specific gene 6 (Gas6) has been extensively used to treat cerebral diseases. This study aimed to evaluate the neuroprotective effects of Gas6 in post-septic mice and to determine the underlying mechanisms of action.
Methods: Mice underwent cecal ligation and puncture (CLP) for sepsis induction. Mice were then immediately injected with 6 µg of Gas6 via the tail vein, and the effect was evaluated after 24 hours. The neurological severity score (NSS) was used to assess neurological deficits in post-septic mice. In addition, brain edema was evaluated by measuring the brain water content and blood-brain barrier (BBB) permeability using Evans blue (EB) dye extravasation. Western blotting and immunofluorescence assays were performed to determine the expression of tight junction (TJ)-associated proteins such as occludin and zonula occludens-1 (ZO-1).
Results: Post-septic mice exhibited increased NSS, brain edema, and BBB permeability. However, acute Gas6 treatment attenuated the severe effects of sepsis on neurologic function in mice. Therefore, Gas6 attenuates brain edema and restores BBB permeability. These findings suggest that Gas6 could alleviate neurological deficits, brain edema, BBB damage, and reverse the decreased expression of occludin and ZO-1 in the brain tissue to protect against SAE.
Conclusion: Gas6 protects against SAE by restoring the impaired BBB permeability.
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