Fig 1.
B. longum BORI (B. BORI) showed a therapeutic effect in OA rats.
(A, C) Pain thresholds were determined by analyses of PWL (time) and PWT (threshold) in MIA-induced OA rats treated with vehicle and B. BORI, respectively, until day 21. (B) Weight-bearing was examined in all groups (n = 6 per group) until day 21. Data are shown as means ± standard errors of the mean (** p < 0.01 and **** p < 0.0001).
Fig 2.
B. longum BORI (B. BORI) reduces bone and cartilage erosion in MIA-induced OA rats.
Rats were injected with 3 mg of MIA. After OA induction, rats were administered B. BORI at 1 × 109 colony-forming units per rat. Rats were sacrificed 21 days after OA induction and joint tissues were collected. (A) Samples from three rats per group were stained with safranin O to determine the Osteoarthritis Research Society International (OARSI) and Mankin scores. (B) Femur samples were scanned via micro-computed tomography (μCT 35; SCANCO Medical, Zurich, Switzerland). Object volume (Obj.V)/total volume (TV) and bone surface were analyzed using NRecon software. Data are shown as means ± standard errors of the mean (* p < 0.05).
Fig 3.
Representative images of immunohistochemical staining for inflammatory mediators in the joint synovium of MIA-induced OA rats treated with B. BORI.
Bar graphs show mean numbers of IL-1β, LTB4r, and PGE2-positive cells in the joint synovium. Data are shown as means ± standard errors of the mean (* p < 0.05 and ** p < 0.01).
Fig 4.
Representative images of immunohistochemical staining for anabolic/catabolic factors in the joint synovium of MIA-induced OA rats treated with B. BORI.
Bar graphs show mean numbers of MMP9 and MMP13-positive cells in the joint synovium. Data are shown as means ± standard errors of the mean (* p < 0.05, ** p < 0.01, and *** p < 0.001).
Fig 5.
B. BORI regulates inflammatory activity and inflammatory apoptosis in chondrocytes.
Human OA chondrocytes were cultured with B. BORI (10 μg/ml) and IL-1β (20 ng/ml) for 24 h. Then, supernatants and cells were collected for analysis. (A) MCP-1 secretion levels were measured in the supernatant of B. BORI-treated OA chondrocytes by enzyme-linked immunosorbent assay. (B) Expression levels of inflammatory cell death mediators after B. BORI treatment were analyzed by quantitative polymerase chain reaction. Data are shown as means ± standard errors of the mean (** p < 0.01 and *** p < 0.001).