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Table · dataset · 2025

<b>Antimicrobial peptide PMAP-36 attenuates ExPEC-induced neuroinflammation by inhibiting the NF-</b><b>κ</b><b>B/NLRP3 pathway through autophagy activation</b>

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<p dir="ltr"><b>Supplementary materials</b></p><p dir="ltr"><b>Figure S1.

Description

The biocompatible effect of PMAP-36 in vitro and in vivo</b>. (A) The viability of BV2 cells treated with PMAP-36 (0.625 μM or 1.25 μM) for 12 h, followed by washing and then incubation for an additional 24 h, was detected via the CCK-8 assay.

Mice (total N=18) were intraperitoneally injected with 5 mg/kg PMAP-36 or PBS as a negative control. (B) Body weight was monitored daily for 7 d, and variations in body weights (%) (total N=12, per group n=6) are shown. (C-F) Blood was collected to determine biochemical indicators, including alanine aminotransferase (ALT) (C), aspartate aminotransferase (AST) (D), urea (UREA) (E) and inorganic phosphate (IP) (F).

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Different tissues (total N=6, per group n=3), including the brain, lung, liver, and spleen, were collected to observe histopathological changes. (G) Representative images of histopathological changes in tissues are shown. All data are presented as the means ± SEM from five, six, or three biological replicates. ns = not significant.</p><p dir="ltr"><b>Figure S2.

The effect of PMAP-36 on bacterial invasion in BV2 cells</b>. (A) The number of intracellular bacteria in ExPEC-infected BV2 cells with PMAP-36 treatment under the condition of 3-MA and CQ at 1 and 2 h post infection. Data are presented as the means ± SEM from three biological replicates. ***<i>P</i> ≤ 0.001, ns = not significant.</p>

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