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Abstract <p>Pressure ulcers (PUs) represent a significant clinical challengein immobilized patients and the aging population, characterizedby persistent inflammation, impaired tissue regeneration, and dysregulated healingprocesses. In this study, we systematically investigated the therapeuticpotential of formononetin (FMN) extracted from traditional Chinesemedicine in preventing and treating PUs. Experimental results fromthe magnetically induced ischemia-reperfusion PUs rat model demonstratedthat FMN intervention accelerated wound healing rates, with a cleardose-response relationship observed. Histopathological examination(H&amp;E staining) revealed substantial improvements in tissue architecture, includingenhanced epidermal integrity and reduced inflammatory infiltration.Moreover, the expression of pro-inflammatory cytokines TNF-α, IL-6,and IL-1β in the wound tissue was reduced. FMN inhibited apoptosisby down-regulating the expression of cleaved caspase-3 and Bax inpressure ulcer tissues and up-regulating the expression of Bcl-2.In addition, FMN promotes collagen deposition and expression ofα-SMA and collagen I in wound tissue, thereby improving tissue remodeling.Integrated bioinformatic and Western blot validation identified simultaneousregulation of NF-κB and PI3K-Akt pathways as the core mechanism.These results reveal that FMN may facilitate PUs healing through dualmechanisms, suppressing inflammation and apoptosis via NF-κB inhibition,and promoting cell survival and tissue repair via PI3K-Akt activation. Thissuggests that FMN has the potential to be a drug for the preventiveand therapeutic effects of PUs and lays the foundation for the clinicaldevelopment of FMN-based treatment options.</p>

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Formononetin Promotes Pressure Ulcer Healing through Coordinated Regulation of NF-κB and PI3K-Akt Signaling Pathways

  • 期刊论文

  • 发表日期：

    2026年6月21日

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  • Haoting Xu,
  • Zhengwen Gao,
  • Yan Lu,
  • Xin Ge,
  • Di Jia,
  • Quanbin Zhou

摘要

Abstract

Pressure ulcers (PUs) represent a significant clinical challengein immobilized patients and the aging population, characterizedby persistent inflammation, impaired tissue regeneration, and dysregulated healingprocesses. In this study, we systematically investigated the therapeuticpotential of formononetin (FMN) extracted from traditional Chinesemedicine in preventing and treating PUs. Experimental results fromthe magnetically induced ischemia-reperfusion PUs rat model demonstratedthat FMN intervention accelerated wound healing rates, with a cleardose-response relationship observed. Histopathological examination(H&E staining) revealed substantial improvements in tissue architecture, includingenhanced epidermal integrity and reduced inflammatory infiltration.Moreover, the expression of pro-inflammatory cytokines TNF-α, IL-6,and IL-1β in the wound tissue was reduced. FMN inhibited apoptosisby down-regulating the expression of cleaved caspase-3 and Bax inpressure ulcer tissues and up-regulating the expression of Bcl-2.In addition, FMN promotes collagen deposition and expression ofα-SMA and collagen I in wound tissue, thereby improving tissue remodeling.Integrated bioinformatic and Western blot validation identified simultaneousregulation of NF-κB and PI3K-Akt pathways as the core mechanism.These results reveal that FMN may facilitate PUs healing through dualmechanisms, suppressing inflammation and apoptosis via NF-κB inhibition,and promoting cell survival and tissue repair via PI3K-Akt activation. Thissuggests that FMN has the potential to be a drug for the preventiveand therapeutic effects of PUs and lays the foundation for the clinicaldevelopment of FMN-based treatment options.