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. 2026 Jan 7;16:1678215. doi: 10.3389/fphar.2025.1678215

Correction: Hesperetin prevents bone resorption by inhibiting RANKL-induced osteoclastogenesis and Jnk mediated Irf-3/c-Jun activation

Qiang Zhang 1, Xinqiao Tang 2, Zhong Liu 2, Xiaoxia Song 3, Dan Peng 1, Wei Zhu 1, Zhengxiao Ouyang 1,*, Wanchun Wang 1,*
PMCID: PMC12820524  PMID: 41573717

There was a mistake in Figure 1C (control and 30 μM groups) as published. During figure preparation, the images for the splenocytes control group and the 30 μM group in Figure 1C were incorrectly selected, resulting in a misrepresentation of the experimental data. The corrected Figure 1 appears below.

FIGURE 1.

Panel A shows osteoclast precursor cell viability after treatment with increasing concentrations of hesperetin, with viability decreasing at higher doses. Panel B presents a dose–response curve used to calculate the IC50 (245.5 μM). Panel C contains representative TRAP-stained images of RAW 264.7 cells, splenocytes, and bone marrow–derived macrophages under RANKL induction with different hesperetin concentrations, alongside bar graphs quantifying TRAP-positive osteoclast number and TRAP-positive area. Panel D shows fluorescence images of F-actin ring formation with quantification of actin ring counts. Panel E shows SEM images of bone resorption.

Non-toxic Hes attenuated RANKL-induced osteoclast formation and function in vitro. (A) Cell viability of osteoclast precursors after Hes treatments for 24 h. (B) Linear correlation between OD values and cell numbers. (C) RANKL-induced osteoclastogenesis after Hes treatments in three types of preosteoclasts, RAW 264.7 cells, splenocytes, and BMMs. (D) Formation of RANKL-induced F-actin rings after Hes treatments. (E) Formation of RANKL-stimulated bone resorption pits after Hes treatments. *p < 0.05 compared with controls, **p < 0.01 compared with controls.

This error does not affect the interpretation or conclusions of the article in any way.

The original article has been updated.

Footnotes

Edited and reviewed by: Peter Vee Sin Lee, The University of Melbourne, Australia

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