Abstract
BackgroundHerbal treatment may have a chondroprotective and therapeutic effect on Osteoarthritis (OA). We investigated the mechanism of action of ginger and curcumin rhizomes cultivated in Egypt in treatment of OA in rat model.MethodsThirty-five albino rats were intra-articularly injected with Monosodium Iodoacetate in the knee joint. Ginger and curcumin was orally administered at doses of 200 and 400 mg/kg (F200 and F400). Serum levels of cartilage oligomeric matrix protein (COMP), hyaluronic acid (HA), malondialdehyde (MDA), myeloperoxidase (MPO), Interleukin-1 beta (IL-1β) and superoxide dismutase activity (SOD) were measured using ELISA. The composition of the herbal formula hydro-ethanolic extract was characterized using UPLC-ESI-MS. Histopathological changes in injected joints was examined using routine histopathology. Statistical analysis was performed using one-way ANOVA.ResultsSerum levels of COMP, HA, MPO, MDA, and IL-1β were significantly decreased in F 200, F 400 and V groups when compared to OA group (P value <0.0001). On the other hand SOD levels were significantly elevated in treated groups compared to OA groups (P value <0.0001).ConclusionsThe ginger/curcumin at 1:1 had chondroprotective effect via anti-inflammatory and antioxidant effect in rat OA model. Further pharmacological and clinical studies are needed to evaluate this effect.
Highlights
Herbal treatment may have a chondroprotective and therapeutic effect on Osteoarthritis (OA)
Effect of herbal formula treatment on blood cartilage oligomeric matrix protein (COMP) Mean serum level of COMP was significantly increased in OA group compared to the control group (P value
The mean serum level of COMP was significantly decreased in F 200, F 400 and V groups when compared to OA group (P value
Summary
Herbal treatment may have a chondroprotective and therapeutic effect on Osteoarthritis (OA). Osteoarthritis (OA) is a common degenerative joint disease in the elderly and a leading cause of physical disability worldwide [1]. It mainly affects the weight– bearing joints, such as hips and knees [2]. A monosodium Iodoacetate (MIA) induced OA model is well described in rats especially in terms of the pathological progression of the disease. The mechanism of action of MIA has been attributed to inhibition of glyceraldehyde-3-phosphate dehydrogenase. This disrupts the glucose metabolism of chondrocytes, leading to reactive oxygen species (ROS) production and caspase
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