Tumor necrosis factor-alpha (TNF-α) has been shown to have an inhibitory effect on the osteogenic differentiation of mesenchymal stem cells. The metabolic switch from glycolysis to oxidative phosphorylation (OXPHOS) is vital for energy supply during osteogenic differentiation. However, the metabolic switch is inhibited under inflammatory stimulation. FGF2 has shown that it can improve osteogenic differentiation and promote autoimmune inflammation. In this study, we investigated whether FGF2 can ameliorate TNF-a-inhibited osteogenic damage by improving OXPHOS. Effects of TNF-α or FGF2 on the proliferation and osteogenic differentiation of hBMSCs were evaluated by MTT assay, qRT-PCR, and ALP activity tests. The function of FGF2 on the TNF-a-inhibited metabolic switch was determined by Mito Stress test. The results showed that TNF-α was able to inhibit the osteogenic differentiation and OXPHOS of hBMSCs. FGF2 has no obvious function in improving the osteogenic-related genes, but it can ameliorate the impaired osteogenesis and OCR value caused by TNF-α. These findings suggest that FGF2 can prevent the impaired osteogenic differentiation and metabolic switch of hBMSCs under inflammatory stimulation, which might enhance the regeneration capacity of hBMSCs.

中文翻译：

---

成纤维细胞生长因子2通过改善氧化磷酸化来改善肿瘤坏死因子-α诱导的人骨间充质干细胞的成骨性损伤。

肿瘤坏死因子-α（TNF-α）已显示对间充质干细胞的成骨分化具有抑制作用。从糖酵解到氧化磷酸化（OXPHOS）的代谢转换对于成骨分化过程中的能量供应至关重要。然而，在炎症刺激下代谢转换受到抑制。FGF2已显示可以改善成骨细胞分化并促进自身免疫炎症。在这项研究中，我们调查了FGF2是否可以通过改善OXPHOS来减轻TNF-a抑制的成骨损伤。通过MTT法，qRT-PCR和ALP活性试验评估TNF-α或FGF2对hBMSCs增殖和成骨分化的影响。通过Mito Stress测试确定FGF2在TNF-α抑制的代谢转换上的功能。结果表明，TNF-α能够抑制hBMSCs的成骨分化和OXPHOS。FGF2在改善成骨相关基因方面没有明显的功能，但可以改善由TNF-α引起的成骨能力和OCR值受损。这些发现表明，FGF2可以预防炎症刺激下hBMSCs的成骨分化和代谢转换受损，这可能增强hBMSCs的再生能力。