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<p>Osteoporosis is a prevalent metabolic bone disease and a significant global health concern, ranking as the fourth major health threat. It is characterized by reduced bone mass and deterioration of bone structure, leading to a higher risk of fractures. This condition is particularly common among women, especially postmenopausal women, due to declining estrogen levels. Osteoporosis-related fractures pose a growing public health challenge, impacting quality of life and placing a substantial burden on healthcare services worldwide. In this study, we examined the efficacy of the phytocompound cnicin in mitigating ovariectomy-induced osteoporosis. Ovariectomy was performed in a rat model, and the rats were treated with two different doses of cnicin. We assessed the impact of cnicin on reproductive organs and weight gain in ovariectomized rats. The effects of cnicin on bone mineral density and bone biomechanics were analyzed in the treated ovariectomized rats. Osteogenic markers, such as estradiol, bone gla protein and acid phosphatase were quantified to evaluate the osteogenic potential of cnicin. The osteogenic effects of cnicin were further confirmed by quantifying osteotrophic markers. Moreover, we measured the signaling proteins of the RANKL/RANK/OPG pathway to assess the impact of cnicin on bone turnover homeostasis. Inflammatory stimulators were quantified to analyze the anti-inflammatory efficacy of cnicin in ovariectomized rats. Cnicin treatment maintained weight gain and increased the weights of reproductive organs in ovariectomized rats. It enhanced bone mineral density and femoral bone strength in these rats. Additionally, estradiol levels increased, while the levels of BGP and ACP decreased in the cnicin-treated ovariectomized rats. Cnicin treatment also regulated osteotrophic markers and RANKL/RANK/OPG pathway signaling proteins in ovariectomized rats. Furthermore, inflammatory stimulators significantly decreased with cnicin treatment in these rats. Overall, our results illustrate that cnicin treatment increases estradiol levels and stimulates osteoblastic activity by regulating the RANKL/RANK/OPG pathway.</p> Graphical Abstract <p></p>

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Cnicin Regulates Bone Turnover Homeostasis in Rats with Ovariectomy-Induced Osteoporosis via RANKL/RANK/OPG Pathway

  • 期刊论文

  • 发表日期：

    2025年5月30日

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  • Ninggang Liao,
  • Zhenming Zeng,
  • Xianghua Pang,
  • Jianfei Zhou,
  • Heng Liao,
  • Zhi Qin,
  • Huaiji Wei,
  • Min Shao

摘要

Osteoporosis is a prevalent metabolic bone disease and a significant global health concern, ranking as the fourth major health threat. It is characterized by reduced bone mass and deterioration of bone structure, leading to a higher risk of fractures. This condition is particularly common among women, especially postmenopausal women, due to declining estrogen levels. Osteoporosis-related fractures pose a growing public health challenge, impacting quality of life and placing a substantial burden on healthcare services worldwide. In this study, we examined the efficacy of the phytocompound cnicin in mitigating ovariectomy-induced osteoporosis. Ovariectomy was performed in a rat model, and the rats were treated with two different doses of cnicin. We assessed the impact of cnicin on reproductive organs and weight gain in ovariectomized rats. The effects of cnicin on bone mineral density and bone biomechanics were analyzed in the treated ovariectomized rats. Osteogenic markers, such as estradiol, bone gla protein and acid phosphatase were quantified to evaluate the osteogenic potential of cnicin. The osteogenic effects of cnicin were further confirmed by quantifying osteotrophic markers. Moreover, we measured the signaling proteins of the RANKL/RANK/OPG pathway to assess the impact of cnicin on bone turnover homeostasis. Inflammatory stimulators were quantified to analyze the anti-inflammatory efficacy of cnicin in ovariectomized rats. Cnicin treatment maintained weight gain and increased the weights of reproductive organs in ovariectomized rats. It enhanced bone mineral density and femoral bone strength in these rats. Additionally, estradiol levels increased, while the levels of BGP and ACP decreased in the cnicin-treated ovariectomized rats. Cnicin treatment also regulated osteotrophic markers and RANKL/RANK/OPG pathway signaling proteins in ovariectomized rats. Furthermore, inflammatory stimulators significantly decreased with cnicin treatment in these rats. Overall, our results illustrate that cnicin treatment increases estradiol levels and stimulates osteoblastic activity by regulating the RANKL/RANK/OPG pathway.

Graphical Abstract