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PAPE-1 ATTENUATES ISCHEMIA-INDUCED NEUROINFLAMMATION VIA NON-NUCLEAR ESTROGEN RECEPTOR SIGNALING
Andrzej Łachand 4 co-authors
Maj Institute of Pharmacology, Polish Academy of Sciences
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS06-09PM-192
Presentation
Date TBA
Board: PS06-09PM-192
Event Information
Poster Board
PS06-09PM-192
Poster
View posterAbstract
The aim of this study was to address the limited repertoire of therapies targeting ischemic stroke, with emphasis on delayed treatment strategies. The limitations of current therapeutic approaches prompted the investigation of Pathway Preferential Estrogen-1 (PaPE-1), a novel estrogenic compound designed to selectively activate non-nuclear estrogen receptor signaling while minimizing adverse hormonal effects. As demonstrated in our previous studies, non-nuclear estrogen receptor activation by PaPE-1 is critically involved in neuroprotection by regulating a broad range of responses following cerebral ischemia, including apoptotic and necrotic cell death pathways, oxidative stress, and cell viability. In the present work, we focused on its involvement in inflammatory processes.
Our research was conducted using mouse primary neocortical neuronal cultures and a human microglial cell line exposed to hypoxia/ischemia, followed by post-treatment with PaPE-1 administered during the reoxygenation phase. Quantitative PCR and ELISA were employed to assess key pro- and anti-inflammatory markers, including interleukins, Cox2, and Nlrp3, which are involved in ischemia-induced neuroinflammation. In addition, we analyzed the expression of inflammation-related microRNAs, including miR-19a, miR-130a, and miR-132. In both experimental models, PaPE-1 significantly attenuated ischemia-induced pro-inflammatory signaling.
In parallel, the effects of PaPE-1 on microglial activation and viability were evaluated using BrdU incorporation, calcein staining, and assessment of morphological changes. PaPE-1 reduced microglial proliferation while preserving cell viability, indicating a direct anti-inflammatory effect. Collectively, these results support targeting non-nuclear estrogen receptors with PaPE-1 as a promising anti-inflammatory therapeutic strategy against ischemic stroke.
Funding: National Science Centre of Poland, grant no 2021/43/D/NZ7/00633.Recommended posters
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