Objective

The aims of the study were to assess the anti-inflammatory properties of platelet-rich plasma (PRP) and investigate its regenerative potential in osteoarthritic (OA) human chondrocytes. We hypothesized that PRP can modulate the inflammatory response and stimulate cartilage regeneration.

Design

Primary human chondrocytes from OA knees were treated with manually prepared PRP, after which cell migration and proliferation were assessed. Next, tumor necrosis factor-α–stimulated chondrocytes were treated with a range of concentrations of PRP. Expression of genes involved in inflammation and chondrogenesis was determined by real-time polymerase chain reaction. In addition, chondrocytes were cultured in PRP gels and fibrin gels consisting of increasing concentrations of PRP. The production of cartilage extracellular matrix (ECM) was assessed. Deposition and release of glycosaminoglycans (GAG) and collagen was quantitatively determined and visualized by (immuno)histochemistry. Proliferation was assessed by quantitative measurement of DNA.

Results

Both migration and the inflammatory response were altered by PRP, while proliferation was stimulated. Expression of chondrogenic markers COL2A1 and ACAN was downregulated by PRP, independent of PRP concentration. Chondrocytes cultured in PRP gel for 28 days proliferated significantly more when compared with chondrocytes cultured in fibrin gels. This effect was dose dependent. Significantly less GAGs and collagen were produced by chondrocytes cultured in PRP gels when compared with fibrin gels. This was qualitatively confirmed by histology.

Conclusions

PRP stimulated chondrocyte proliferation, but not migration. Also, production of cartilage ECM was strongly downregulated by PRP. Furthermore, PRP did not act anti-inflammatory on chondrocytes in an in vitro inflammation model.

中文翻译：

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尽管增殖增加，但富含血小板的血浆在体外不会抑制炎症或促进人骨关节炎软骨细胞的再生。

客观的

该研究的目的是评估富含血小板的血浆 (PRP) 的抗炎特性，并研究其在骨关节炎 (OA) 人软骨细胞中的再生潜力。我们假设 PRP 可以调节炎症反应并刺激软骨再生。

设计

用人工制备的 PRP 处理来自 OA 膝关节的原代人软骨细胞，然后评估细胞迁移和增殖。接下来，用一系列浓度的 PRP 处理肿瘤坏死因子-α 刺激的软骨细胞。通过实时聚合酶链反应确定参与炎症和软骨形成的基因的表达。此外，软骨细胞在 PRP 凝胶和由增加浓度的 PRP 组成的纤维蛋白凝胶中培养。评估了软骨细胞外基质 (ECM) 的产生。糖胺聚糖 (GAG) 和胶原蛋白的沉积和释放通过（免疫）组织化学进行定量测定和可视化。通过DNA的定量测量评估增殖。

结果

PRP 改变了迁移和炎症反应，同时刺激了增殖。软骨形成标志物 COL2A1 和 ACAN 的表达被 PRP 下调，与 PRP 浓度无关。与在纤维蛋白凝胶中培养的软骨细胞相比，在 PRP 凝胶中培养 28 天的软骨细胞增殖明显更多。这种效果是剂量依赖性的。与纤维蛋白凝胶相比，在 PRP 凝胶中培养的软骨细胞产生的 GAG 和胶原蛋白显着减少。组织学定性地证实了这一点。

结论

PRP 刺激软骨细胞增殖，但不刺激迁移。此外，PRP 强烈下调了软骨 ECM 的产生。此外，在体外炎症模型中，PRP 对软骨细胞没有抗炎作用。