Fig 1: Representative images of in vivo biodegradation of EPO-PLGA-PEG after post-crush injury administration. EPO-PLGA-PEG was administered directly onto the 3 mm sciatic nerve crush site, as shown by the arrows, on day 0. On post-injury day 14, blood vessels were abundant at the injection and peri-injection site post-injury, forming a microvascular network. The gel was still present on the nerve on day 21 (n = 5/group; scale bar = 1 mm)
Fig 2: Effects of EPO-PLGA-PEG on motor and sensory functional outcomes post-crush injury. A EPO-PLGA-PEG significantly improved SFI on days 3, 7, and 14 compared to saline and vehicle groups. B EPO-PLGA-PEG significantly improved grip strength on days 3, 7, 14, and 21 post-injury compared to saline. C EPO-PLGA-PEG significantly improved withdrawal reflex (percent response to filament) as compared to saline on post-injury days 3, 7, and 14 (n = 5/group; mean ± SEM; *p < 0.05, **p < 0.01, and ***p < 0.001 vs. saline group; ssp < 0.01 and sssp < 0.001 vs. PLGA-PEG group)
Fig 3: Effect of EPO-PLGA-PEG on whole-mount nerve fiber distribution post-crush injury. A Representative NF-H-stained whole-mount images to display nerve fibers. B Quantification of NF-H integrated density (n = 5/group; mean ± SEM; **p < 0.01 vs. saline group; sp < 0.05 and ssp < 0.01 vs. PLGA-PEG group; #p < 0.05 and ##p < 0.01 vs. uninjured group; scale bar = 100 µm). Each image represents 3 images from 5 different SNs, for a total of 15 images analyzed per group
Fig 4: Release kinetics and CD spectroscopy of EPO-PLGA-PEG. A Percent of total encapsulated EPO from PLGA-PEG hydrogels (n = 3/group; mean ± SEM). B CD spectroscopy of released EPO at different time intervals from PLGA-PEG hydrogels (n = 3/group)
Fig 5: Schematic representation of an EPO-loaded thermogel as a local controlled-release delivery system
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