Shan Lu
Yun Luo
GuiBo Sun
XiaoBo Sun- 1Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China
- 2Institute of Medicinal Plant Development, Beijing Key Laboratory of Innovative Drug Discovery of Traditional Chinese Medicine (Natural Medicine) and Translational Medicine, Beijing, China
- 3Key Laboratory of Bioactive Substances and Resource Utilization of Chinese Herbal Medicine, Ministry of Education, Beijing, China
- 4Key Laboratory of Efficacy Evaluation of Chinese Medicine Against Glyeolipid Metabolism Disorder Disease, State Administration of Traditional Chinese Medicine, Beijing, China
- 5Key Laboratory of New Drug Discovery Based on Classic Chinese Medicine Prescription, Chinese Academy of Medical Sciences, Beijing, China
by Lu S, Luo Y, Sun G and Sun X (2020). Front. Pharmacol. 11:567238. doi: 10.3389/fphar.2020.567238
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.
“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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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.
Edited and reviewed by:
Galina Sud’ina, Lomonosov Moscow State University, RussiaCopyright © 2025 Lu, Luo, Sun and Sun. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: GuiBo Sun, c3VuZ3VpYm9AMTI2LmNvbQ==; XiaoBo Sun, c3VuX3hpYW9ibzE2M0AxNjMuY29t
†These authors have contributed equally to this work