Oral administration of soybean okara extract reduces osteoarthritis pain and progression in rats

Abstract

Osteoarthritis (OA) is a common inflammatory degenerative disease that causes joint pain and irreversible bone damage, affecting many middle-aged and elderly people. Currently, there is no effective treatment available. Okara, a byproduct of soybean processing, contains bioactive compounds with antioxidant and anti-inflammatory properties similar to those found in soybeans, making it a promising candidate for reuse as a food supplement to provide health benefits. In this study, we explored the therapeutic potential of soybean okara extract (SOE) in OA using a rat surgical anterior cruciate ligament transection (ACLT) OA model. Oral administration of SOE significantly alleviated bone pain associated with ACLT, as demonstrated by a weight-bearing behavioral assay. Histopathological analysis revealed that oral SOE ameliorated ACLT-induced bone destruction, improved cartilage and synovium integrity, and reduced the levels of proinflammatory cytokines IL-1β, TNF-α, and the chondrolytic enzyme MMP-3. This, in turn, led to a decrease in the degradation of aggrecan and collagen type II, thereby preserving cartilage. These findings suggest that oral administration of SOE could be a promising approach for the prevention and treatment of OA.

Keywords: anti-inflammatory agents, osteoarthritis; antioxidant; soybean okara.

Figure 1

(A) Schematic diagram of experiment design. (B) Growth curve of body weight throughout the experimental period. No significant variations were observed between the study groups.

Figure 2

Oral SOE decelerates ACLT-induced bone pain. The pain behavior weight-bearing test suggests that rats of the ACLT+SOE and the positive control ACLT+Celecoxib groups were in less pain than ACLT group (*p < 0.05). #p < 0.05 ACLT vs. no surgery control group.

Figure 3

Oral SOE ameliorates osseous damage in the ACLT-induced OA knee joint. (A) Micro-CT images of rat right knee joints of control, ACLT and ACLT+SOE and ACLT+Celecoxib groups at transverse and coronal views. Red arrows indicate the bone loss. (B-H) Quantitative analyses of the BMD (B), BMC (C), (BV/TV (D), BS/TV (E), Tb.N (F), Tb.Th (G), and Tb.Sp (H) data in all study groups. # p < 0.05 vs. control group; * p < 0.05 vs. ACLT group.

Figure 4

Oral SOE ameliorates cartilage degradation in the ACLT-induced OA knee joint. (A&B) Histopathological analysis of ACLT-induced OA knee articular cartilage damage in by Safranin-O/Fast Green (A) and H&E (B) staining. Scale bar = 500 μm. Assessment of osteoarthritic cartilage histopathology by OARSI (C), synovial membrane inflammation (D) and cartilage degeneration (E, arrow heads or red box) scores show less cartilage damage in oral SOE and celecoxib groups compared to ACLT group (* p < 0.05). # p < 0.05 vs. control group. Abbreviations: ST, synovial tissue; CA, cartilage; SH, synovial hyperplasia (arrows).

Figure 5

Oral SOE suppress the induction of IL-1β and TNF-α in ACLT-induced OA articular cartilage. Immuno-histochemistry analysis and scoring of IL-1β (A, B) and TNF-α (A, C) in rat right knee joint cartilage. Scale bar = 100 μm. # p<0.05 vs. control group. * p<0.05 vs. ACLT group.

Figure 6

Oral SOE reserve the expression of aggrecan and collagen II accompanying with suppression of MMP3 in ACLT-induced OA articular cartilage. (A) Immuno-histochemistry analysis MMP3, aggrecan and collagen II in rat right knee joint cartilage. Scale bar = 100 μm. (B-D) Scoring of the immunosignals of MMP3 (B), aggrecan (C) and collagen II (D) in and scoring of MMP3, aggrecan and collagen II. # p<0.05 vs. control group. * p<0.05 vs. ACLT group.