Department of Orthopedics, The First Affiliated Hospital of Wannan Medical College, Yijishan Hospital, No. 2, Zhe Shan Xi Road, Wuhu 241001, Anhui, China; Anhui Province Key Laboratory of Non-coding RNA Basic and Clinical Transformation, No. 2, Zhe Shan Xi Road, Wuhu 241001, Anhui, China.
Department of Orthopedics, The First Affiliated Hospital of Wannan Medical College, Yijishan Hospital, No. 2, Zhe Shan Xi Road, Wuhu 241001, Anhui, China.
Int Immunopharmacol. 2024 Dec 25;143(Pt 2):113420. doi: 10.1016/j.intimp.2024.113420. Epub 2024 Oct 26.
Paederosidic acid (PA) has shown beneficial effects in anti-inflammatory studies, but it is unclear whether PA has positive impacts on bone loss induced by lipopolysaccharide (LPS). This study aims to investigate the influence of PA on bone loss in LPS-treated rats. The study assesses changes in the viability and osteogenic potential of MC3T3-E1 cells, as well as osteoclast differentiation in RAW264.7 cells in the presence of LPS using CCK-8, ALP staining, AR staining, and Tartrate-resistant acid phosphatase (TRAP) staining. In vitro experiments indicate that LPS-induced inhibition of osteoclasts (OC) and Superoxide Dismutase 2 (SOD2) correlates with heightened levels of inflammation and oxidative stress. Furthermore, PA has demonstrated the ability to alleviate oxidative stress and inflammation, enhance osteogenic differentiation, and suppress osteoclast differentiation. Animal experiments also show that PA significantly upregulates SOD2 expression while downregulating TNF-α expression (all, p < 0.05), leading to the restoration of impaired bone metabolism, improved bone strength, and increased bone mineral density (all, p < 0.05), compared to the control group. The collective experimental findings strongly suggest that PA can enhance osteogenic activity in the presence of LPS by reducing inflammation and oxidative stress, hindering osteoclast differentiation; hence mitigating bone loss in LPS-treated rat models.
漆酚（PA）在抗炎研究中显示出有益的效果，但尚不清楚 PA 是否对脂多糖（LPS）诱导的骨丢失有积极影响。本研究旨在探讨 PA 对 LPS 处理大鼠骨丢失的影响。该研究使用 CCK-8、ALP 染色、AR 染色和耐酒石酸酸性磷酸酶（TRAP）染色评估 LPS 存在时 MC3T3-E1 细胞活力和成骨潜能以及 RAW264.7 细胞破骨细胞分化的变化。体外实验表明，LPS 诱导的破骨细胞（OC）和超氧化物歧化酶 2（SOD2）抑制与炎症和氧化应激水平升高有关。此外，PA 已被证明能够减轻氧化应激和炎症，增强成骨分化，并抑制破骨细胞分化。动物实验还表明，PA 可显著上调 SOD2 表达，同时下调 TNF-α 表达（均 p<0.05），从而恢复受损的骨代谢，增强骨强度，并增加骨密度（均 p<0.05），与对照组相比。总的实验结果强烈表明，PA 可以通过减少炎症和氧化应激，抑制破骨细胞分化，从而减轻 LPS 处理大鼠模型中的骨丢失，增强 LPS 存在时的成骨活性。
