Department of Rehabilitation Medicine, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, People's Republic of China.
BMC Musculoskelet Disord. 2024 May 9;25(1):331. doi: 10.1186/s12891-024-07437-7.
The development of neuropathic pain (NP) is one of the reasons why the pain is difficult to treat, and microglial activation plays an important role in NP. Recently, platelet-rich plasma (PRP) has emerged as a novel therapeutic method for knee osteoarthritis (KOA). However, it's unclarified whether PRP has analgesic effects on NP induced by KOA and the underlying mechanisms unknown.
To observe the analgesic effects of PRP on NP induced by KOA and explore the potential mechanisms of PRP in alleviating NP.
KOA was induced in male rats with intra-articular injections of monosodium iodoacetate (MIA) on day 0. The rats received PRP or NS (normal saline) treatment at days 15, 17, and 19 after modeling. The Von Frey and Hargreaves tests were applied to assess the pain-related behaviors at different time points. After euthanizing the rats with deep anesthesia at days 28 and 42, the corresponding tissues were taken for subsequent experiments. The expression of activating transcription factor 3 (ATF3) in dorsal root ganglia (DRG) and ionized-calcium-binding adapter molecule-1(Iba-1) in the spinal dorsal horn (SDH) was detected by immunohistochemical staining. In addition, the knee histological assessment was performed by hematoxylin-eosin (HE) staining.
The results indicated that injection of MIA induced mechanical allodynia and thermal hyperalgesia, which could be reversed by PRP treatment. PRP downregulated the expression of ATF3 within the DRG and Iba-1 within the SDH. Furthermore, an inhibitory effect on cartilage degeneration was observed in the MIA + PRP group only on day 28.
These results indicate that PRP intra-articular injection therapy may be a potential therapeutic agent for relieving NP induced by KOA. This effect could be attributed to downregulation of microglial activation and reduction in nerve injury.
神经病理性疼痛（NP）的发展是疼痛难以治疗的原因之一，小胶质细胞激活在 NP 中起着重要作用。最近，富血小板血浆（PRP）作为一种治疗膝骨关节炎（KOA）的新方法出现。然而，PRP 是否对 KOA 引起的 NP 具有镇痛作用以及潜在机制尚不清楚。
观察 PRP 对 KOA 引起的 NP 的镇痛作用，并探讨 PRP 缓解 NP 的潜在机制。
在第 0 天向雄性大鼠膝关节腔内注射单碘乙酸钠（MIA）诱导 KOA。造模后第 15、17 和 19 天，大鼠分别接受 PRP 或 NS（生理盐水）治疗。在不同时间点应用 Von Frey 和 Hargreaves 测试评估疼痛相关行为。在第 28 和 42 天用深麻醉处死大鼠后，取相应组织进行后续实验。免疫组织化学染色检测背根神经节（DRG）中激活转录因子 3（ATF3）和脊髓背角（SDH）中离子钙结合衔接分子 1（Iba-1）的表达。此外，通过苏木精-伊红（HE）染色进行膝关节组织学评估。
结果表明，MIA 注射诱导机械性痛觉过敏和热痛觉过敏，PRP 治疗可逆转这种情况。PRP 下调 DRG 中的 ATF3 和 SDH 中的 Iba-1 的表达。此外，仅在第 28 天，MIA+PRP 组观察到对软骨退变的抑制作用。
这些结果表明，PRP 关节内注射治疗可能是缓解 KOA 引起的 NP 的潜在治疗剂。这种作用可能归因于小胶质细胞激活的下调和神经损伤的减少。
