The Journal of Practical Medicine >

2026 , Vol. 42 >Issue 13: 2444 - 2453

DOI: https://doi.org/10.3969/j.issn.1006-5725.2026.13.021

Treatise：Mechanism and Practice

Ferulic acid improves delayed wound healing caused by arsenic poisoning by inhibiting NF-κB signaling

  • Yuxiu LI ,
  • Zhe YANG ,
  • Zhenfen ZHANG ,
  • Binwei XU ,
  • Yan HONG
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  • Department of Histology and Embryology，School of Basic Medicine，Guizhou Medical University，Guiyang 561113，Guizhou，China

Received date: 2026-04-29

  Online published: 2026-07-14

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Abstract

Objective To investigate the therapeutic effect and the underlying mechanism of ferulic acid （FA） on the delayed wound healing induced by arsenic poisoning in a mouse skin wound model. Methods （1） Male C57BL/6 mice were administered drinking water containing NaAsO2 for 3 months to establish an arsenic poisoning model. （2） Full-thickness skin defects were created on the backs of normal and arsenic-poisoned mice. Subsequently， normal saline or FA solution was topically applied. The mice were divided into four groups： the control group， the FA group， the NaAsO2 group， and the NaAsO2+FA group. Wound healing was evaluated through photographic monitoring. Wound tissues were collected for HE staining and Masson staining to assess the degree of healing. Inflammatory factors were detected by Real-time PCR， and the expression levels of tight junction proteins （Claudin-1 and Occludin） as well as key proteins of the nuclear factor κB （NF-κB） pathway （p65 and P-p65） were measured by Western blot. （3） Human umbilical vein endothelial cells （HUVECs） were divided into four groups： the control group， the NaAsO2 group， the NaAsO2+FA group， and the FA group. The study aimed to verify the effects of NaAsO? on the proliferation and migration capabilities of HUVECs， as well as on the expression of inflammatory factors， tight junction proteins， and the NF-κB pathway. Results （1） When compared to the control group， the NaAsO? group in mice demonstrated significantly slower wound healing （P 0.05）. Additionally， there was a decrease in the expression of collagen fibers and tight-junction proteins in the wound tissues （P 0.05）， an increase in the expression of inflammatory factors （P 0.05）， and activation of the NF-κB pathway （P 0.05）. In contrast to the NaAsO? group， the NaAsO?+FA group showed accelerated wound healing （P 0.05）， an elevation in the expression of collagen fibers and tight-junction proteins （P 0.05）， a reduction in the expression of inflammatory factors （P 0.05）， and inhibition of the NF-κB pathway （P 0.05）. （2） In HUVEC cells， stimulation with NaAsO? significantly inhibited cell proliferation and migration （P 0.05）， down-regulated the expression of tight-junction proteins （P 0.05）， promoted the expression of inflammatory factors， and activated the NF-κB signaling pathway （P 0.05）. The combined intervention with FA could significantly reverse the adverse effects induced by NaAsO? （P 0.05）. Conclusion FA can inhibit the inflammatory response by suppressing the NF-κB signaling pathway and upregulate the expression of tight junction proteins， which in turn improves the delayed wound healing caused by arsenic poisoning.

Key words： arsenic poisoning; ferulic acid; delayed wound healing; tight junctions; NF-κB pathway; inflammatory response; human umbilical vein endothelial cells

Cite this article

Yuxiu LI , Zhe YANG , Zhenfen ZHANG , Binwei XU , Yan HONG . Ferulic acid improves delayed wound healing caused by arsenic poisoning by inhibiting NF-κB signaling[J]. The Journal of Practical Medicine, 2026 , 42(13) : 2444 -2453 . DOI: 10.3969/j.issn.1006-5725.2026.13.021

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