Figure 8
Inhibition of PRP-regenerative activity by ASA is partially compensated for by optimisation. Four round full-thickness excisional wounds, 3 mm in diameter, were generated in the back skin of female BALB/c mice (8–10 weeks old). PRPr or O-PRPr obtained from ASA- or non-ASA- treated mice was injected into the wounds generated in ASA-treated mice. Injection with saline was used as the control. The healing process was analysed at 3, 7, and 10 days post-injury. (A) Wounds were photographed, and the perimeter of the wound area was determined using the ImageJ software and expressed as a percentage of the area on day 0. (B) Skin biopsies were obtained at day 10 and stained with Masson’s trichrome. Images were captured using an inverted microscope. (C) Epidermal thickness, (D) granulation tissue volume (dotted lines), (E) immature blood microvessels containing intraluminal erythrocytes, and (F) annex structures (hair follicles and sebaceous glands) were quantified using the ImageJ software. (Magnification 100X, n = 7; *P < 0.05, **P < 0.01, ***P < 0.001 vs. control; #P < 0.05, ##P < 0.01 vs. PRPr; ‡P < 0.05, ‡‡P < 0.01 vs. the same treatment without ASA).
