Abstract
Osteoarthritis (OA) has become one of the most common disabilities among elders, especially in females. Obesity and mechanical injuries caused by OA are attributed to joint loading, cartilage disintegration, and bone loss, as well as inflammation. Pharmacological and non-pharmacological treatments can be used for OA. Fucoidan possesses several bioactivities such as antitumor, antiviral, anticoagulation, anti-obesity, and immunomodulation. This study aims to investigate the effect of fucoidan in surgery-induced OA on rats with diet-induced obesity. OA was induced by an anterior cruciate ligament transection and a partial medial meniscectomy (ACLT + MMx). The male SD rats were fed with a high-fat diet (HFD) for 4 weeks to induce obesity before causing ACLT + MMx to induce OA. The OA rats were administered with intragastric water or fucoidan in three different concentrations (32 mg/kg, 64 mg/kg, and 320 mg/kg) after the surgeries for 40 days with an HFD. We observed that the swelling in the knee joint was alleviated and the hind paw weight distribution was rectified after feeding them with fucoidan and that there was no significant effect on the weight gain and feed intake. Fucoidan administration indicated no significant variation on the high-density lipoprotein (HDL)-Cholesterol level, but it did indicate reduced plasma triglycerides and low-density lipoprotein (LDL)-Cholesterol levels. In addition, the weight-bearing tests showed an improvement in the fucoidan-treated group. Our results suggested that fucoidan may improve meniscal/ligamentous injury and obesity-induced OA.
Highlights
Osteoarthritis (OA) is the most prevalent form of arthritis [1]
We observed that the swelling in the knee joint was alleviated and the hind paw weight distribution was rectified after feeding them with fucoidan and that there was no significant effect on the weight gain and feed intake
The body weights of high-fat diet (HFD)-induced obese rats were significantly increased compared to the sham group (p < 0.05)
Summary
OA is one of the most common chronic health conditions and a leading cause of disability and pain among adults [2]. OA has an inflammatory component affecting the synovium and cartilage, which leads to subchondral bone tissue breakdown, resulting in pain, stiffness, and joint failure [3,4,5]. OA joint degeneration occurs from a combination of mechanical stresses and biochemical factors [4,6]. Chondrocytes as well as synovial cells, in an elevated OA condition, express inflammatory cytokines such as interleukin (IL)-1β and the tumor necrosis factor (TNF)-α. There is an increase in the matrix metalloproteinase (MMPs) and some pro-inflammatory cytokines such as IL-8, IL-6, prostaglandin E2, and nitric oxide [5]
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