Front. Pharmacol.Frontiers in PharmacologyFront. Pharmacol.1663-9812Frontiers Media S.A.149924210.3389/fphar.2025.1499242PharmacologyCorrectionCorrection: Ginsenoside compound K attenuates Ox-LDL-mediated macrophage inflammation and foam cell formation via autophagy induction and modulating NF-κB, p38, and JNK MAPK signalingLu et al.10.3389/fphar.2025.1499242LuShan12345†LuoYun12345†SunGuiBo12345*SunXiaoBo12345*1Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China2Institute of Medicinal Plant Development, Beijing Key Laboratory of Innovative Drug Discovery of Traditional Chinese Medicine (Natural Medicine) and Translational Medicine, Beijing, China3Key Laboratory of Bioactive Substances and Resource Utilization of Chinese Herbal Medicine, Ministry of Education, Beijing, China4Key Laboratory of Efficacy Evaluation of Chinese Medicine Against Glyeolipid Metabolism Disorder Disease, State Administration of Traditional Chinese Medicine, Beijing, China5Key Laboratory of New Drug Discovery Based on Classic Chinese Medicine Prescription, Chinese Academy of Medical Sciences, Beijing, China
Edited and reviewed by:Galina Sud’ina, Lomonosov Moscow State University, Russia
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A Correction On 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 by Lu S, Luo Y, Sun G and Sun X (2020). Front. Pharmacol. 11:567238. doi: 10.3389/fphar.2020.567238atherosclerosisginsenoside compound Kinflammationautophagymacrophagesection-at-acceptanceInflammation Pharmacology
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.
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.
Diagram with four panels: A shows a chemical structure of a compound; B is a bar graph illustrating cell viability at various CK concentrations in micrograms per milliliter; C displays microscope images under different conditions including control and ox-LDL with varying CK concentrations; D is another bar graph displaying oil-red-O levels comparing control, ox-LDL, and CK treatments at different microgram concentrations.
“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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