ArticleBasic and clinical neuroscience2025
Intranasal Autologous Conditioned Serum Attenuates Memory Impairment After mPFC Ischemia in Mice.
Article in Basic and clinical neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Globally, stroke ranks as the second most prevalent cause of death, contributing significantly to worldwide mortality burdens, imposing a significant economic and emotional challenge on societies. This study was designed to investigate the effect of autologous conditioned serum (ACS) on memory and associated molecular factors in a mouse model of photothrombotic ischemic stroke. Methods: The photothrombotic model was used to induce medial prefrontal cortex (mPFC) ischemia. ACS were prepared by intracardiac puncture of C57BL/6 mice using special ACS syringes. After blood incubation, the sample was centrifuged, and the serum was analyzed with ELISA kits to quantify the levels of interleukin-1 receptor antagonist (IL-1RA) and insulin-like growth factor (IGF-I). The ischemic animals received 48 μL intranasal ACS two times a day, once a day, or once every other day for one week. Behavioral tests, including the Lashley-III maze and social interaction test, were conducted following treatment administration. Additionally, IGF-1, IL-1β, IL-1RA levels, and phospho-tau/total-tau ratio were measured in the mPFC area by western blot. Histological analysis was performed to assess ischemic volume. Results: The results indicated that once-daily administration of ACS significantly improved spatial memory in the Lashley-III maze and showed a notable enhancement in social memory as measured by the social interaction test. In terms of molecular analysis, ACS increased the levels of IGF-1 and IL-1RA, whilst decreasing the levels of IL-1β and p-tau/total-tau ratio. Conclusion: In conclusion, post-stroke intranasal ACS administration enhances memory, possibly by increasing the level of IGF-1 and attenuating inflammation through the inhibition of IL-1β signal by IL-1RA, and regulation of tau levels.
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