Fig. 7

L-PRP produces greater inflammatory responses than P-PRP. Quantification of inflammatory marker gene expression was performed by using quantitative reverse transcription-polymerase chain reaction (a). Gene expression of IL-1β, IL-6, and TNF-α were upregulated by L-PRP. But P-PRP upregulated only TNF-α, downregulated IL-6, and did not have a significant effect on IL-1β gene expression (a). The control group was used as the reference (1-fold). Data are represented as mean ± SD of three independent values. Additionally, the levels of IL-1β, IL-6, and TNF-α were measured by using enzyme-linked immunosorbent assay (b). The concentration of each cytokine in each group was normalized to its cell number. L-PRP significantly increased IL-1β and IL-6 protein levels but did not have a significant effect on TNF-α production. P-PRP did not affect IL-1β, increased IL-6, and decreased TNF-α protein levels in tenocytes differentiated from tendon stem/progenitor cells. Asterisks indicate significant differences between each PRP treatment and the respective control group (P < 0.05). Pound symbols represent significant differences between L-PRP- and P-PRP-treated groups (P < 0.05). Note that, for each group, three independent values were measured from three experiments, and the results are expressed as the mean ± SD. A t test was used for statistical analysis. IL interleukin, L-PRP leukocyte-platelet-rich plasma, P-PRP pure-platelet-rich plasma, SD standard deviation, TNF-α tumor necrosis factor-alpha