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Fig. 6 | Molecular Medicine

Fig. 6

From: Pretreatment with platelet-rich plasma protects against ischemia–reperfusion induced flap injury by deactivating the JAK/STAT pathway in mice

Fig. 6

Evaluating the expression of proteins involved in the JAK/STAT pathway and apoptosis in I/R-injured skin flaps after PRP treatment. A Protein expression was measured by Western blotting using skin flap samples after PRP treatment in I/R-injured mice. β-actin served as an internal equal loading control. The ratios of B p-JAK2/JAK2, C p-STAT1/STAT1, and D p-STAT3/STAT3 were generated to determine the activation of JAK/STAT pathway. The relative protein levels of anti-apoptotic E Bcl-2 and F Bcl-xL, as well as pro-apoptotic G Bax were also quantified and present in bar graphs. Error bars represent the means ± SD (n = 4). Student’s t-test for comparison between two groups, and one-way ANOVA followed by the Tukey–Kramer post hoc test for comparison among multiple groups were used. *p < 0.05 vs. the corresponding PBS control, &p < 0.05 vs. the value in pre-PRP group after I/R insult, #p < 0.05 vs. the value in mid-PRP group after I/R insult. In each bargraph, the white bars from left to right represented treatment with PBS without I/R insult, before I/R insult, before reperfusion, or after reperfusion, respectively; the slash bar represented treatment with PRP without I/R insult; the black bar represented treatment with PRP before I/R insult; the dark grey bar represented treatment with PRP before reperfusion; the light grey bar represented treatment with PRP after reperfusion

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