Department of Orthopedics, The First Affiliated Hospital of Nanchang University, Artificial Joints Engineering and Technology Research Center of Jiangxi Province, Nanchang, Jiangxi Province 330006, China.
Department of General Practice, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Int Immunopharmacol. 2023 Apr;117:109884. doi: 10.1016/j.intimp.2023.109884. Epub 2023 Feb 17.
Fractures caused by osteoporosis (OP) are one of the main causes of death in the elderly, bringing a heavy burden to the country and society. The imbalance between osteoblast-mediated osteogenesis and osteoclast-mediated bone resorption is an important cause of OP. Therefore, finding drugs that can regulate this dynamic balance can be an important way to treat osteoporosis. Surfactin is a highly effective biosurfactant derived from Bacillus subtilis and it has been proven to have various pharmacological effects in previous studies, but its effect on bone metabolism remains unknown. Here, we performed a study on the role and mechanism of Surfactin in inhibiting osteoclastogenesis and its possible mechanism as well as the role in promoting osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs).
We investigated the effect of Surfactin on osteoclast differentiation and osteogenic differentiation in vitro and in vivo. The effect of Surfactin on the activity of osteoclastogenesis and osteogenesis was verified by CCK-8 assay, quantitative Real-time polymerase chain reaction (qPCR) and Western blotting analysis were used to verify the effect of Surfactin on osteoclast and osteogenic differentiation-specific genes and proteins. The effect of Surfactin on TRAP、ALP activity and mineral deposition was verified by TRAP、ALP and ARS staining. We then used an ovariectomy-induced osteoporosis mice model to observe the effect of Surfactin in vivo.
Surfactin is noncytotoxic to BMMs, RAW264.7, and BMSCs. And it can effectively inhibit osteoclastogenesis and promote osteogenic differentiation. Moreover, we found that Surfactin can inhibit the differentiation of osteoclasts through the NF-κB signaling pathway. Surfactin can also alleviate bone loss in ovariectomy-induced osteoporosis mice.
Our results suggest that Surfactin can inhibit osteoclastogenesis through the NF-κB signaling pathway, promote the osteogenic differentiation of BMSCs, and also can effectively alleviate bone loss in ovariectomy-induced osteoporosis mice.
骨质疏松症（OP）引起的骨折是老年人死亡的主要原因之一，给国家和社会带来了沉重的负担。成骨细胞介导的成骨作用和破骨细胞介导的骨吸收之间的失衡是 OP 的一个重要原因。因此，寻找可以调节这种动态平衡的药物可能是治疗骨质疏松症的重要途径。表面活性剂是一种从枯草芽孢杆菌中提取的高效生物表面活性剂，在之前的研究中已被证明具有多种药理作用，但它对骨代谢的影响尚不清楚。在这里，我们研究了表面活性剂在抑制破骨细胞分化中的作用和机制及其在促进骨髓间充质干细胞（BMSCs）成骨分化中的可能作用。
我们研究了表面活性剂在体外和体内对破骨细胞分化和成骨分化的影响。通过 CCK-8 测定、定量实时聚合酶链反应（qPCR）和 Western blot 分析验证了表面活性剂对破骨细胞和成骨分化特异性基因和蛋白的活性的影响。通过 TRAP、ALP 和 ARS 染色验证了表面活性剂对 TRAP、ALP 活性和矿物质沉积的影响。然后，我们使用去卵巢诱导骨质疏松症小鼠模型观察表面活性剂的体内作用。
表面活性剂对 BMMs、RAW264.7 和 BMSCs 无细胞毒性。它可以有效抑制破骨细胞分化，促进成骨分化。此外，我们发现表面活性剂可以通过 NF-κB 信号通路抑制破骨细胞的分化。表面活性剂还可以减轻去卵巢诱导骨质疏松症小鼠的骨丢失。
我们的结果表明，表面活性剂可以通过 NF-κB 信号通路抑制破骨细胞分化，促进 BMSCs 的成骨分化，并且可以有效缓解去卵巢诱导骨质疏松症小鼠的骨丢失。
