Lin Qing, Ouyang Xinchen, Pan Qi, Huang Jiajia, Zhang Zhifen, Yang Yumei, Wang Haoyu, Yang Li, Zhu Xiaofeng, Li Xiaoyun, Zhang Ronghua
College of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong, China.
Guangdong Provincial Key Laboratory of Traditional Chinese Medicine Informatization, Guangzhou, Guangdong, China.
Planta Med. 2025 Mar;91(3):127-141. doi: 10.1055/a-2462-4844. Epub 2024 Nov 5.
Drynariae Rhizoma has been commonly used as a preventive and therapeutic agent for bone diseases. However, its pharmacological mechanisms have not been fully elucidated. Here, we aimed to investigate the effects of Drynariae Rhizoma in a bilateral ovariectomized rat model and explore the correlation with gut microbiome. We established an ovariectomized rat model, which we treated with different doses of Drynariae Rhizoma (Drynariae Rhizoma-Low, 0.27 g/kg/day; Drynariae Rhizoma-Middle, 0.81 g/kg/day; Drynariae Rhizoma-High, 2.43 g/kg/day) through intragastric administration for 12 weeks. Results showed that Drynariae Rhizoma alleviated body weight, moderated bone microstructure, and promoted the expression of bone formation-related factors in ovariectomized rats, in which Drynariae Rhizoma-High showed the most significant effects among the three doses. Furthermore, the effects of Drynariae Rhizoma on promoting bone formation were correlated to the changes in microbial richness and the restorations of several genera, among which and were positively correlated with the bone formation-related factors, and both were enriched in the Drynariae Rhizoma-High group as biomarkers. Moreover, CMP-legionaminate biosynthesis I might be a crucial pathway of Drynariae Rhizoma to regulate gut microbiota. The content of serum short-chain fatty acids in the ovariectomized rats were regulated by Drynariae Rhizoma. Our results demonstrate that Drynariae Rhizoma promotes bone formation in ovariectomized rats, and is related to the regulation of the gut microbiota structure.
骨碎补一直被广泛用作骨疾病的预防和治疗药物。然而,其药理机制尚未完全阐明。在此,我们旨在研究骨碎补在双侧卵巢切除大鼠模型中的作用,并探讨其与肠道微生物群的相关性。我们建立了卵巢切除大鼠模型,通过灌胃给予不同剂量的骨碎补(低剂量骨碎补,0.27 g/kg/天;中剂量骨碎补,0.81 g/kg/天;高剂量骨碎补,2.43 g/kg/天),持续12周。结果表明,骨碎补可减轻去卵巢大鼠的体重,改善骨微结构,并促进骨形成相关因子的表达,其中高剂量骨碎补在三种剂量中效果最为显著。此外,骨碎补促进骨形成的作用与微生物丰富度的变化以及几个菌属的恢复有关,其中[菌属1]和[菌属2]与骨形成相关因子呈正相关,且在高剂量骨碎补组中均作为生物标志物富集。此外,CMP - 军团菌酸生物合成I可能是骨碎补调节肠道微生物群的关键途径。骨碎补可调节去卵巢大鼠血清短链脂肪酸的含量。我们的结果表明,骨碎补可促进去卵巢大鼠的骨形成,并与肠道微生物群结构的调节有关。