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<p>Osteoarthritis (OA) is a long-term chronic, progressive degenerative joint disease characterized via cartilage degradation, subchondral bone remodeling and synovial inflammation, finally leading to joint dysfunction and pain. Aromadendrin, a natural flavonoid has been reported to possess potent antioxidant and anti-inflammatory effect in different pathological conditions. This current study investigates the protective effects of aromadendrin against monoiodoacetate (MIA)-induced OA in rats and explore the underlying mechanism. OA was induced in the rodent via intra-articular administration of MIA (3&#xa0;mg/50 µL sterile saline), following OA induction, the rats received the oral administration of aromadendrin and diclofenac sodium for 8&#xa0;weeks. Body weight and joint diameter were estimated at regular intervals. Metabolic parameters such as food intake, water intake, urine output, and fecal output, were monitored throughout the study. End of the study, bone metabolism markers, antioxidant parameters, hepatic, non-hepatic parameters, inflammatory cytokines, inflammatory parameters, apoptosis parameters, and mRNA expression were estimated. Aromadendrin significantly improved the body weight and suppressed the joint diameters at different time intervals (week 2, 4, 6, and 8). Aromadendrin significantly suppressed the level of bone parameters such as COMP, CTX-II, aggrecan, and collagen type II. Aromadendrin altered the food intake, water intake, urine output, fecal output along with oxidative stress (MDA, SOD, CAT, GSH, GPx); inflammatory cytokines (TNF-α, IL-1β, IL-4, IL-6, IL-10, IL-18); inflammatory parameters (COX-2, iNOS, PGE2, NF-κB); apoptosis parameters (Bax. Bcl-2, caspase-3) and MMP level (MMP-1, MMP-2, MMP-3, MMP-9). Aromadendrin significantly altered the mRNA expression of HO-1, Nrf<sub>2</sub>, Bax, Bcl-2, caspase-3, TLR4, MyD88, and NF-κB. The finding of this study demonstrates the protective effect of aromadendrin against MIA-induced OA in the rats via alteration of TLR4/MyD88/NF-κB, HO-1/Nrf2, and Bcl-2/Caspase-3 pathways.</p> Graphical Abstract <p></p>

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Protective effect of aromadendrin against monoiodoacetate-induced osteoarthritis in rats via modulation of TLR4/MyD88/NF-κB, HO-1/Nrf2, and Bcl-2/Caspase-3 signaling pathways

  • 期刊论文

  • 发表日期：

    2026年1月12日

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  • Jie Wang,
  • Pengcheng Wang

摘要

Osteoarthritis (OA) is a long-term chronic, progressive degenerative joint disease characterized via cartilage degradation, subchondral bone remodeling and synovial inflammation, finally leading to joint dysfunction and pain. Aromadendrin, a natural flavonoid has been reported to possess potent antioxidant and anti-inflammatory effect in different pathological conditions. This current study investigates the protective effects of aromadendrin against monoiodoacetate (MIA)-induced OA in rats and explore the underlying mechanism. OA was induced in the rodent via intra-articular administration of MIA (3 mg/50 µL sterile saline), following OA induction, the rats received the oral administration of aromadendrin and diclofenac sodium for 8 weeks. Body weight and joint diameter were estimated at regular intervals. Metabolic parameters such as food intake, water intake, urine output, and fecal output, were monitored throughout the study. End of the study, bone metabolism markers, antioxidant parameters, hepatic, non-hepatic parameters, inflammatory cytokines, inflammatory parameters, apoptosis parameters, and mRNA expression were estimated. Aromadendrin significantly improved the body weight and suppressed the joint diameters at different time intervals (week 2, 4, 6, and 8). Aromadendrin significantly suppressed the level of bone parameters such as COMP, CTX-II, aggrecan, and collagen type II. Aromadendrin altered the food intake, water intake, urine output, fecal output along with oxidative stress (MDA, SOD, CAT, GSH, GPx); inflammatory cytokines (TNF-α, IL-1β, IL-4, IL-6, IL-10, IL-18); inflammatory parameters (COX-2, iNOS, PGE2, NF-κB); apoptosis parameters (Bax. Bcl-2, caspase-3) and MMP level (MMP-1, MMP-2, MMP-3, MMP-9). Aromadendrin significantly altered the mRNA expression of HO-1, Nrf2, Bax, Bcl-2, caspase-3, TLR4, MyD88, and NF-κB. The finding of this study demonstrates the protective effect of aromadendrin against MIA-induced OA in the rats via alteration of TLR4/MyD88/NF-κB, HO-1/Nrf2, and Bcl-2/Caspase-3 pathways.

Graphical Abstract