Department of Rehabilitation Medicine, Hubei Provincial Hospital, Wuhan 430071, China.
Department of Rehabilitation medicine, Wuhan Fourth Hospital, Wuhan 430033, China.
Tissue Cell. 2022 Aug;77:101830. doi: 10.1016/j.tice.2022.101830. Epub 2022 May 21.
Osteoarthritis (OA), also known as degenerative osteoarthritis, has a complex etiology, and its pathogenesis remains unclear. Platelet-rich plasma (PRP) therapy has been widely used in medicine and other related professions since its clinical application was first reported in the 1980 s and the 1990 s. This study aimed to investigate the effects and potential mechanisms of PRP in OA. An in vitro model of osteoarthritis was constructed by lipopolysaccharide (LPS) stimulation, and the effect of PRP on LPS-induced chondrocytes was evaluated. The results indicated that although LPS inhibited chondrocyte proliferation and promoted inflammation and apoptosis, these effects were reversed by PRP. In addition, the LPS-suppressed expression of aggrecan, TGF-β, PDGF, and COL2A1 was restored by PRP, whereas the LPS-enhanced expression of MMP3 was suppressed by PRP. Furthermore, PRP inhibited LPS-induced mitochondrial damage by suppressing reactive oxygen species production, mitochondrial permeability transition pore opening, Drp1 expression, and upregulating Mfn1 expression. In addition, PRP inhibited the phosphorylation of AMPK and NF-κB. Collectively, this study indicates that PRP might be a potential therapeutic candidate for the treatment of OA by repairing mitochondrial function through the activation of AMPK/NF-κB signaling.
骨关节炎（OA），又称退行性骨关节炎，其病因复杂，发病机制尚不清楚。富血小板血浆（PRP）治疗自上世纪 80 年代和 90 年代首次报道临床应用以来，已广泛应用于医学和其他相关专业。本研究旨在探讨 PRP 在 OA 中的作用及潜在机制。通过脂多糖（LPS）刺激构建骨关节炎体外模型，评估 PRP 对 LPS 诱导的软骨细胞的作用。结果表明，虽然 LPS 抑制软骨细胞增殖，促进炎症和细胞凋亡，但 PRP 逆转了这些作用。此外，PRP 恢复了 LPS 抑制的聚集蛋白聚糖、TGF-β、PDGF 和 COL2A1 的表达，而抑制了 LPS 增强的 MMP3 表达。此外，PRP 通过抑制活性氧产生、线粒体通透性转换孔开放、Drp1 表达和上调 Mfn1 表达抑制 LPS 诱导的线粒体损伤。此外，PRP 抑制 AMPK 和 NF-κB 的磷酸化。综上所述，本研究表明，PRP 通过激活 AMPK/NF-κB 信号通路修复线粒体功能，可能成为治疗 OA 的潜在治疗候选药物。
