Andia Isabel, Rubio-Azpeitia Eva, Maffulli Nicola
Regenerative medicine Group, Biocruces Health Research Institute, Cruces University Hospital, 48903, Barakaldo, Spain.
Clin Orthop Relat Res. 2015 May;473(5):1624-34. doi: 10.1007/s11999-015-4179-z.
Platelet-rich plasma therapies for tendinopathy appear to provide moderate pain reduction. However, the biological mechanisms behind the observed clinical effects remain poorly characterized.
QUESTIONS/PURPOSES: The purpose of this study was to explore whether platelet-rich plasma modifies the inflammatory/angiogenic status of already inflamed tenocytes by examining (1) gene expression; (2) modulation of chemokine and interleukin secretion; and (3) differences between healthy and tendinopathic tenocytes.
Cells from both healthy and tendinopathic tendons were exposed to interleukin (IL)-1ß and after treated with platelet-rich plasma. Modifications in the expression of selected genes were assessed by real-time reverse transcription-polymerase chain reaction and changes in secretion of angiogenic/inflammatory molecules by enzyme-linked immunosorbent assay. Platelet-rich plasma-induced changes in tendinopathic cells were compared with normal after normalizing platelet-rich plasma data against IL-1ß status in each specific sample.
In IL-1ß-exposed cells, platelet-rich plasma downregulates expression of IL-6/CXCL-6 (mean, 0.015; 95% confidence interval [CI], 0.005-0.025; p = 0.026), IL-6R (mean, 0.61; 95% CI, 0.27-0.95; p = 0.029), and IL-8/CXCL-8 (mean, 0.02; 95% CI, 0.007-0.023; p = 0.026). Secretion of IL-6/CXCL6, 0.35 (95% CI, 0.3-0.4; p = 0.002), IL-8/CXCL8, 0.55 (95% CI, 0.5-0.7; p = 0.01), and monocyte chemoattractant protein-1/CCL2, 0.40 (95% CI, 0.2-0.6; p = 0.001) was reduced by platelet-rich plasma, whereas vascular endothelial growth factor increased by twofold, (95% CI, 1.7-2.3; p < 0.001). RANTES/CCL5 increased by10-fold (95% CI, 4-17) and hepatocyte growth factor by 21-fold (95% CI, 0.2-42) in tendinopathic and by 2.3-fold (95% CI, 2-3) and threefold (95% CI, 1-5) in normal cells (p = 0.005 for both).
Platelet-rich plasma induces an immunomodulatory and proangiogenic phenotype consistent with healing mechanisms with few differences between tendinopathic and normal cells.
Platelet-rich plasma injections in pathological and nearby tissue might help to recover tendon homeostasis.
富血小板血浆疗法对肌腱病似乎有一定程度的疼痛缓解作用。然而，所观察到的临床效果背后的生物学机制仍不清楚。
问题/目的：本研究的目的是通过检测（1）基因表达；（2）趋化因子和白细胞介素分泌的调节；（3）健康和肌腱病性肌腱细胞之间的差异，来探讨富血小板血浆是否会改变已发炎的肌腱细胞的炎症/血管生成状态。
将来自健康和肌腱病性肌腱的细胞暴露于白细胞介素（IL）-1β，然后用富血小板血浆处理。通过实时逆转录-聚合酶链反应评估所选基因表达的变化，并通过酶联免疫吸附测定评估血管生成/炎症分子分泌的变化。在将每个特定样本中富血小板血浆数据相对于IL-1β状态进行标准化后，将富血小板血浆诱导的肌腱病性细胞变化与正常细胞进行比较。
在暴露于IL-1β的细胞中，富血小板血浆下调IL-6/CXCL-6（平均值，0.015；95%置信区间[CI]，0.005 - 0.025；p = 0.026）、IL-6R（平均值，0.61；95%CI，0.27 - 0.95；p = 0.029）和IL-8/CXCL-8（平均值，0.02；95%CI，0.007 - 0.023；p = 0.026）的表达。富血小板血浆使IL-6/CXCL6的分泌减少，为0.35（95%CI，0.3 - 0.4；p = 0.002），IL-8/CXCL8的分泌减少，为0.55（95%CI，0.5 - 0.7；p = 0.01），单核细胞趋化蛋白-1/CCL2的分泌减少，为0.40（95%CI，0.2 - 0.6；p = 0.001），而血管内皮生长因子增加了两倍，（95%CI，1.7 - 2.3；p < 0.001）。在肌腱病性细胞中，调节激活正常T细胞表达和分泌的趋化因子/CCL5增加了10倍（95%CI，4 - 17），肝细胞生长因子增加了21倍（95%CI，0.2 - 42），在正常细胞中分别增加了2.3倍（95%CI，2 - 3）和3倍（95%CI，1 - 5）（两者p = 0.
