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. 2026 Apr 22;17:1774570. doi: 10.3389/fphar.2026.1774570

Correction: Edaravone plays protective effects on LPS-induced microglia by switching M1/M2 phenotypes and regulating NLRP3 inflammasome activation

Jiping Li 1, Xinping Dai 2, Liuyi Zhou 3, Xinxiu Li 4, Dongxiao Pan 1,*
PMCID: PMC13147359  PMID: 42100319

There was a mistake in Figure 6A as published. The resolution of the immunofluorescence image was insufficient and did not meet the required quality for clear presentation. The corrected Figure 6 appears below.

FIGURE 6.

Panel A shows fluorescent microscopy images of cells stained for NLRP3 (green) and nuclei (DAPI, blue) under five conditions: control, EDA, LPS, LPS plus EDA at 25 micromolar, and LPS plus EDA at 50 micromolar. Increased NLRP3 staining is visible with LPS, reduced by EDA co-treatment. Panel B presents western blot bands for NLRP3, caspase-1, ASC, and beta-actin from the same conditions, with corresponding bar graphs quantifying protein levels. LPS increases protein expression; EDA co-treatment decreases it in a dose-dependent manner. Statistical comparisons are indicated.

EDA Inhibited NLRP3 inflammasome activation in vitro. BV-2 cells were treated with EDA for 1 h followed by the application of LPS (100 ng/mL) for 24 h. (A) Immunofluorescence detection of NLRP3 inflammasome in BV-2 cells were performed. Scale bar = 10 μm. (B) The protein expressions of NLRP3, ASC and caspase-1 were detected by Western blot assay. The ratio of densitometry values of NLRP3, ASC and caspase-1 with β-actin were assessed and normalized to each respective control cultures. Data were the mean ± SEM from six independent experiments performed in triplicate. ***p < 0.001 compared with control cultures; #p < 0.05, #p < 0.01 compared with LPS-treated cultures.

The original article has been updated.

Footnotes

Edited and reviewed by: Matilde Otero-Losada, National Scientific and Technical Research Council (CONICET), Argentina

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