Departments of Orthopaedics and Otorhinolaryngology, Erasmus MC, Dr. Molewaterplein 50, Rotterdam, the Netherlands.
Am J Sports Med. 2011 Nov;39(11):2362-70. doi: 10.1177/0363546511419278. Epub 2011 Aug 19.
Platelet-rich plasma (PRP) has recently been postulated as a treatment for osteoarthritis (OA). Although anabolic effects of PRP on chondrocytes are well documented, no reports are known addressing effects on cartilage degeneration. Since OA is characterized by a catabolic and inflammatory joint environment, the authors investigated whether PRP was able to counteract the effects of such an environment on human osteoarthritic chondrocytes.
Platelet-rich plasma inhibits inflammatory effects of interleukin-1 (IL-1) beta on human osteoarthritic chondrocytes.
Controlled laboratory study.
Human osteoarthritic chondrocytes were cultured in the presence of IL-1 beta to mimic an osteoarthritic environment. Medium was supplemented with 0%, 1%, or 10% PRP releasate (PRPr, the active releasate of PRP). After 48 hours, gene expression of collagen type II alpha 1 (COL2A1), aggrecan (ACAN), a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)4, ADAMTS5, matrix metalloproteinase (MMP)13, and prostaglandin-endoperoxide synthase (PTGS)2 was analyzed. Additionally, glycosaminoglycan (GAG) content, nitric oxide (NO) production, and nuclear factor kappa B (NFκB) activation were studied.
Platelet-rich plasma releasate diminished IL-1 beta-induced inhibition of COL2A1 and ACAN gene expression. The PRPr also reduced IL-1 beta-induced increase of ADAMTS4 and PTGS2 gene expression. ADAMTS5 gene expression and GAG content were not influenced by IL-1 beta or additional PRPr. Matrix metalloproteinase 13 gene expression and NO production were upregulated by IL-1 beta but not affected by added PRPr. Finally, PRPr reduced IL-1 beta-induced NFκB activation to control levels containing no IL-1 beta.
Platelet-rich plasma releasate diminished multiple inflammatory IL-1 beta-mediated effects on human osteoarthritic chondrocytes, including inhibition of NFκB activation.
Platelet-rich plasma releasate counteracts effects of an inflammatory environment on genes regulating matrix degradation and formation in human chondrocytes. Platelet-rich plasma releasate decreases NFκB activation, a major pathway involved in the pathogenesis of OA. These results encourage further study of PRP as a treatment for OA.
富血小板血浆（PRP）最近被认为是治疗骨关节炎（OA）的一种方法。虽然 PRP 对软骨细胞的合成代谢作用已有充分的文献记载，但目前还没有关于其对软骨退变影响的报道。由于 OA 的特征是分解代谢和炎症性关节环境，作者研究了 PRP 是否能够对抗这种环境对人 OA 软骨细胞的影响。
富血小板血浆抑制白细胞介素-1（IL-1）β对人 OA 软骨细胞的炎症作用。
对照实验室研究。
用 IL-1β培养人 OA 软骨细胞，模拟 OA 环境。培养基中添加 0%、1%或 10% PRP 释放剂（PRPr，PRP 的活性释放剂）。48 小时后，分析胶原 II 型 α1（COL2A1）、聚集蛋白聚糖（ACAN）、解整合素和金属蛋白酶与凝血酶 3 型（ADAMTS）4、ADAMTS5、基质金属蛋白酶（MMP）13 和前列腺素内过氧化物合酶（PTGS）2 的基因表达。此外，还研究了糖胺聚糖（GAG）含量、一氧化氮（NO）产生和核因子 kappa B（NFκB）的激活。
PRP 释放剂减轻了 IL-1β诱导的 COL2A1 和 ACAN 基因表达抑制。PRPr 还降低了 IL-1β诱导的 ADAMTS4 和 PTGS2 基因表达的增加。ADAMTS5 基因表达和 GAG 含量不受 IL-1β或额外的 PRPr 的影响。IL-1β上调了 MMP13 基因表达和 NO 产生，但不受添加的 PRPr 的影响。最后，PRPr 将 IL-1β诱导的 NFκB 激活降低至不含 IL-1β的对照水平。
PRP 释放剂减轻了多种炎症性 IL-1β介导的对人 OA 软骨细胞的作用，包括抑制 NFκB 激活。
PRP 释放剂对抗炎症环境对人类软骨细胞基质降解和形成相关基因的影响。PRP 释放剂降低 NFκB 激活，这是 OA 发病机制中的一个主要途径。这些结果鼓励进一步研究 PRP 作为 OA 的治疗方法。
