Fig. 6: SA intra-articular injection ameliorates ACLT-induced OA progression.

a Diagram summarizing the animal experiments. ACLT was used to construct the knee OA model. Four weeks later, intra-articular injection of SA-loaded PLGA was performed, and intra-articular injection of PLGA only was used as a control. Four weeks after treatment, rats in each group were sacrificed, and knee joints were subjected to histological analysis. b H&E and safranin O/green staining for each treatment group. H&E (upper panel) and safranin O/green staining (lower panel) showed that ACLT resulted in thicker cartilage and degeneration of the cartilage matrix than sham treatment, and intra-articular injection of SA-loaded PLGA ameliorated this progression compared with vehicle (PLGA only) treatment or sham treatment. OARSI scoring (ii) and cartilage matrix area quantitative analysis (iii) showed that, although OARSI scores in the ACLT, vehicle and SA groups were significantly higher than that of the sham group, the OARSI score in the SA group was significantly lower than those of the ACLT and vehicle groups (n = 5, one-way ANOVA). c Ki67 staining for detecting chondrocyte proliferation. IF staining was used to detect Ki67-positive chondrocytes in each treatment group (i). Quantitative analysis showed that SA dramatically promoted chondrocyte Ki67 expression compared with ACLT (n = 5, one-way ANOVA). d TUNEL staining for detecting chondrocyte apoptosis. TUNEL staining showed that SA treatment reversed ACLT-induced chondrocyte apoptosis (i). Quantitative analysis showed the same trend (ii) (n = 5, one-way ANOVA). ACLT group indicates the group with PBS injection; vehicle group indicates the group injected with only PLGA vehicle; SA group indicates the group injected with SA-loaded PLGA. Dashed lines indicate the cartilage surface. Scale bar 50 μm, data are expressed as the mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001, and ns, not significant.