European journal of pharmacology · 2026
Coixol attenuates osteoclastogenesis and ovariectomy-induced bone loss via the HIF-1α-mediated suppression of NF-κB signaling.
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Shi Shu-Wen, Fu Yi-Fei, Wu Xian, Wang Lei-Sheng, Zhang Zhen-Yu, Luo Zi-Xin, Wu Jun-Jie, Yuan Zheng-Dong, Nie Hao, Zhang Ke-Yue, Ti Hui-Bo, Hu Hai-Ting, Qian Yi-Qing, Wang Xin-Chen, Yao Xing-Chen, Peng Tao, Li Xia, Yuan Feng-Lai, Ye Jun-Xing
Аннотация
BACKGROUND: Osteoporosis is a common metabolic bone disease characterized by an imbalance in bone remodeling, which leads to elevated bone resorption due to enhanced osteoclastic activity. Current anti-resorptive therapies are limited by adverse effects and suboptimal efficacy. Coixol, a natural compound derived from the traditional edible plant Coix lacryma-jobi L., exhibits anti-inflammatory properties. However, its role in osteoporosis remains unclear.
METHODS: The effects of coixol on osteoclast formation and function during receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclastogenesis were examined in bone marrow-derived macrophages. Differentiation was evaluated using tartrate-resistant acid phosphatase staining and F-actin ring formation assays, whereas bone resorption activity was quantified using pit formation assays. The expression levels of osteoclast-associated markers (NFATc1, CTSK, and MMP9) and hypoxia-inducible factor 1-alpha (HIF-1α) were assessed using reverse transcription quantitative real-time polymerase chain reaction and Western blot assays. In vivo efficacy in an ovariectomized mouse model was determined using micro-computed tomography and histomorphometric analyses.
RESULTS: Coixol dose-dependently inhibited osteoclast differentiation, disrupted F-actin ring formation, and decreased bone resorption activity, and these activities were accompanied by the downregulation of key osteoclastogenic genes and proteins. Under normoxic conditions, coixol increased HIF-1α protein levels. In ovariectomized mice, coixol significantly attenuated bone loss, improved trabecular bone microstructure, and suppressed osteoclast activity.
CONCLUSION: Coixol likely inhibits osteoclast formation and bone resorption in vitro and in vivo by activating HIF-1α and suppressing nuclear factor-kappa B pathway signaling. These findings suggest that coixol, acting through an HIF-1α-mediated mechanism, could be a potential natural therapeutic agent for osteoporosis.
METHODS: The effects of coixol on osteoclast formation and function during receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclastogenesis were examined in bone marrow-derived macrophages. Differentiation was evaluated using tartrate-resistant acid phosphatase staining and F-actin ring formation assays, whereas bone resorption activity was quantified using pit formation assays. The expression levels of osteoclast-associated markers (NFATc1, CTSK, and MMP9) and hypoxia-inducible factor 1-alpha (HIF-1α) were assessed using reverse transcription quantitative real-time polymerase chain reaction and Western blot assays. In vivo efficacy in an ovariectomized mouse model was determined using micro-computed tomography and histomorphometric analyses.
RESULTS: Coixol dose-dependently inhibited osteoclast differentiation, disrupted F-actin ring formation, and decreased bone resorption activity, and these activities were accompanied by the downregulation of key osteoclastogenic genes and proteins. Under normoxic conditions, coixol increased HIF-1α protein levels. In ovariectomized mice, coixol significantly attenuated bone loss, improved trabecular bone microstructure, and suppressed osteoclast activity.
CONCLUSION: Coixol likely inhibits osteoclast formation and bone resorption in vitro and in vivo by activating HIF-1α and suppressing nuclear factor-kappa B pathway signaling. These findings suggest that coixol, acting through an HIF-1α-mediated mechanism, could be a potential natural therapeutic agent for osteoporosis.