Fig. 7: CEL-PRNPs reduce the number of OCs and inflammatory macrophages in joints of rats with advanced arthritis.

a TUNEL immunofluorescence staining in ankle joints from AIA rats receiving the indicated treatment (Scale bar = 200 μm) (n = 5 independent animals). b Immunohistochemical analyses of the TRAP-stained OCs and CD68-stained synovial macrophages in the joint tissues from rats receiving the indicated treatment (Scale bar = 100 μm) (n = 5 independent animals). c RANKL/OPG ratio in arthritic joints, IL-1β secretion in blood, and TNF secretion in blood from rats receiving the indicated treatment. Data represent mean ± SD (n = 5 independent animals). Statistical significance was determined by a two-sided Student’s t test. d Detection of IL-1β, TNF, OCN, and ALP expression levels in arthritic joints in different groups. Arthritic joints in different groups were stained with IL-1β, TNF, and OCN antibodies, respectively. ALP was stained light–dark in arthritic joints from different groups (Scale bar = 100 μm) (n = 5 independent animals). CEL celastrol CEL-NPs CEL-loaded poly (d, l-lactide-co-glycolide) (PLGA) nanoparticles, CEL-RNPs CEL-loaded RGD peptide-modified PLGA nanoparticles, CEL-PRNPs CEL-loaded matrix metalloproteinase 9 (MMP9)-cleavable polyethylene glycol (PEG)- and RGD peptide-modified PLGA nanoparticles, TUNEL TdT-mediated dUTP nick end labeling, TRAP tartrate-resistant acid phosphatase, RANKL receptor of activator of NF-kB ligand, OPG osteoprotegerin, IL-1β interleukin-1 β, TNF tumor necrosis factor, OCN osteocalcin, ALP alkaline phosphatase.