Fig. 5: Microglial activation affects astrocytic inflammation and EAAT1 expression through extracellular vesicle-mediated signaling. | Communications Biology

Fig. 5: Microglial activation affects astrocytic inflammation and EAAT1 expression through extracellular vesicle-mediated signaling.

From: Astrocytic EAAT1 suppression by EV-ACLY underlies glutamate imbalance and cognitive impairment in POCD

Fig. 5: Microglial activation affects astrocytic inflammation and EAAT1 expression through extracellular vesicle-mediated signaling.The alternative text for this image may have been generated using AI.

A Schematic illustration of experimental design for co-culture experiments. Astrocytic C8-D1A cells were co-cultured with BV2/BV2M1(activated with LPS, 2 μg/ml for 48 h)/BV2M1 + GW4869 for 48 h. The downstream analyses included Western blot, annexin V/PI assay and immunofluorescence staining for p65 and EAAT1. Created in BioRender. Ding, L. (2026) https://BioRender.com/g1hk8n9. B Western blot analysis comparing ACLY protein level in C8-D1A after co-cultured with BV2, BV2M1, or BV2M1 + GW4869. **p < 0.01, n = 5 independent biological replicates; all values represent mean ± standard deviation, one-way ANOVA with Newman–Keuls multiple comparison test. C Flow cytometry analysis (annexin V/PI) assessing cell viability and apoptosis in C8-D1A cells after co-cultured with BV2, BV2M1 or BV2M1 + GW4869. D Immunofluorescence staining of C8-D1A cells for NF-κB p65 (green), glutamate transporter EAAT1 (red), and nuclei (DAPI, blue) in different groups. Scale bar: 50 μm. E Fluorescence intensity profiles for p65, EAAT1 and nuclear-to-cytoplasmic ratio of p65 in C8-D1A co-cultured with BV2, BV2M1, or BV2M1 + GW4869. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.001, n = 5; all values represent mean ± standard deviation, one-way ANOVA with Newman–Keuls multiple comparison test.

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