CORRECTION article

Front. Pharmacol., 17 June 2025

Sec. Inflammation Pharmacology

Volume 16 - 2025 | https://doi.org/10.3389/fphar.2025.1499242

Correction: Ginsenoside compound K attenuates Ox-LDL-mediated macrophage inflammation and foam cell formation via autophagy induction and modulating NF-κB, p38, and JNK MAPK signaling

  • 1. Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China

  • 2. Institute of Medicinal Plant Development, Beijing Key Laboratory of Innovative Drug Discovery of Traditional Chinese Medicine (Natural Medicine) and Translational Medicine, Beijing, China

  • 3. Key Laboratory of Bioactive Substances and Resource Utilization of Chinese Herbal Medicine, Ministry of Education, Beijing, China

  • 4. Key Laboratory of Efficacy Evaluation of Chinese Medicine Against Glyeolipid Metabolism Disorder Disease, State Administration of Traditional Chinese Medicine, Beijing, China

  • 5. Key Laboratory of New Drug Discovery Based on Classic Chinese Medicine Prescription, Chinese Academy of Medical Sciences, Beijing, China

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In the published article, there was an error in the legend for Figure 1 as published. In Figure 1D, it was an error to state that oil red O positive area was measured by Image J software. The corrected legend appears below.

FIGURE 1

“CK inhibited ox-LDL-induced RAW264.7 cells lipid accumulation. RAW264.7 cells were treated with CK at various concentrations for 12 h with or without 80 μg/mL ox-LDL for additional 24 h. (A) The chemical formula for CK. (B) Cell viability was assayed by the MTT assay. (C) Representative images of Oil Red O staining. (D) OD value results of oil red O. All data are shown as mean ± SD from three independent experiments with each performed in triplicate. #P < 0.05, ##P < 0.01 vs. control group; **P < 0.01 vs. ox-LDL-treated group. CK, compound K; ox-LDL, oxidized low-density lipoprotein; MTT, (4, 5-dimethylthiazol-2yl-)-2,5-diphenyl tetrazolium bromide.”

In the published article, there was an error in Figure 1 as published. In Figure 1C, the representative picture of the CK group was updated with the correct one. The corrected Figure 1 and its caption appear above.

In the published article, there was an error in the legend for Figure 6 as published. In Figure 6D, it was an error to state that oil red O positive area was measured by Image J software. The corrected legend appears below.

“CK mediated-autophagy and anti-inflammation were abolished by NF-κB, P38, and JNK MAPK activation. RAW264.7 cells were treated with CK (1.25 μg/mL) for 12 h with or without the NF-κB inhibitor, PDTC (10 μM) or the MAPK activator, anisomycin (0.1 μM) or the autophagy inhibitor 3-MA (5 mM). Then cells were stimulated with 80 μg/mL ox-LDL for 24 h. (A) The protein expression levels of LC3, Beclin-1, P62, IL-1β, TNF-α, and β-actin were examined by western blot assay. (B) Statistical results of LC3II/LC3I, Beclin-1, P62, IL-1β, and TNF-α expression levels. (C) Representative images of Oil Red O staining. (D) OD value results of oil red O. (E) Representative Western blot analysis of phosphorylated and total p38, and JNK was performed. (F) The expression levels of LC3, Beclin-1, P62, IL-1β, TNF-α, and β-actin were detected by Western blot analysis. (G) Densitometric analysis was used to quantify the levels of p-p38, p-JNK. (H) Statistical results of LC3II/LC3I, Beclin-1, P62, IL-1β, and TNF-α expression levels. All data are shown as mean ± SD from three independent experiments with each performed in triplicate. #P < 0.05, ##P < 0.01, ###P < 0.001 vs. control group; *P < 0.05, **P < 0.01, ***P < 0.001 vs. ox-LDL-treated group; &P < 0.05, &&P < 0.01 vs. ox-LDL and CK treatment group. CK, compound K; PDTC, pyrrolidinedithiocarbamate ammonium; 3-MA, 3-Methyladenine; AM, anisomycin.”

The original version of this article has been updated.

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Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Summary

Keywords

atherosclerosis, ginsenoside compound K, inflammation, autophagy, macrophage

Citation

Lu S, Luo Y, Sun G and Sun X (2025) Correction: Ginsenoside compound K attenuates Ox-LDL-mediated macrophage inflammation and foam cell formation via autophagy induction and modulating NF-κB, p38, and JNK MAPK signaling. Front. Pharmacol. 16:1499242. doi: 10.3389/fphar.2025.1499242

Received

20 September 2024

Accepted

06 June 2025

Published

17 June 2025

Volume

16 - 2025

Edited and reviewed by

Galina Sud’ina, Lomonosov Moscow State University, Russia

Updates

Copyright

*Correspondence: GuiBo Sun, ; XiaoBo Sun,

†These authors have contributed equally to this work

Disclaimer

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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