In recent years, Osteoarthritis (OA) has become one of the most common disorders among the elderly, especially women. Articular cartilage covering the joint surface mainly includes chondrocytes, extra-articular type 2 collagen, and proteoglycan (glycoprotein). Articular cartilage has no blood circulation or nerve fiber distribution.
Cartilage degeneration and wear occur due to mechanical stimulation and similar causes of arthropathy. Additionally, inflammation of the synovial membrane surrounding the joint also occurs, accelerating deterioration.
It may also be accompanied by proliferative changes such as periarticular osteochondral formation. These changes cause joint capsule fibrosis accompanied by hypervascularity and nerve fiber hyperplasia, making it easier to feel pain. Also, obesity and mechanical damage caused by OA result from joint loading, cartilage breakdown, bone loss, and inflammation.
However, there is a promising solution. Fucoidan extracted from Cladosiphon okamuranus contains several biological activities such as anti-tumor, anti-viral, anti-coagulant, anti-obesity, and immunomodulatory.
In this blog, I would like to introduce the study that aimed to investigate the effect of Fucoidan in surgery-induced OA in rats with diet-induced obesity.
First, in the study” Effect of Fucoidan on Anterior Cruciate Ligament Transection and Medial Meniscectomy Induced Osteoarthritis in High-Fat Diet-Induced Obese Rats,” by Sabri Sudirman et al., OA was induced by anterior cruciate ligament transection and partial medial meniscectomy (ACLT + MMx).
A male SD rat was fed a high-fat diet (HFD) for four weeks to induce obesity and then ACLT + MMx to generate her OA. OA rats were also checked daily for general postoperative health, pain, discomfort, and infection. Cefazolin (20 mg/kg i.p.) was injected after surgery to prevent infection. After surgery, various doses of Fucoidan were administered intragastrically to rats.
After 40 days of surgery on HFD, three different concentrations (32 mg/kg, 64 mg/kg, and 320 mg/kg) were administered with intragastric water or Fucoidan. ACLT + MMx-treated joints were swollen for an extended period due to OA-induced inflammation. Treatment with Fucoidan helped reduce swelling as the difference in knee width between both hindlimbs decreased over time. (See Figure 1b) The swelling in joints was corrected, but no significant effect was observed on body weight gain and food intake.
Although high-density lipoprotein (HDL)-cholesterol levels were not reduced, plasma triglyceride and low-density lipoprotein (LDL)-cholesterol levels were shown to be reduced.
Furthermore, weight-bearing tests showed that OA surgery significantly differed in the forces exerted by both hindlimbs. On the other hand, oral administration of Fucoidan protected weight bearing in his HFD-induced rats with ALCT + MMx-induced OA. Fucoidan was reported to exhibit a protective effect against monosodium iodide acetate (MIA)-induced OArat.
Similarly, fucoidan supplementation decreased leptin and IL-1β levels, the production of pro-inflammatory cytokines associated with chronic systemic inflammation primarily caused by obesity. Plasma inflammatory cytokines, particularly TNF-α and leptin, were raised in HFD-fed rats, whereas fucoidan supplementation decreased leptin and IL-1β levels. (See Figure 2) Treatment with Fucoidan reduces inflammatory cytokines in plasma compared to the untreated group given HFD. The results suggest that Fucoidan may ameliorate meniscal/ligament injuries and obesity-induced OA.
