astaxanthine and Osteoarthritis

Osteoarthritis is a significant global health problem. Many patients seek more effective alternatives to nonsteroidal anti-inflammatory medicines or commercial supplements to manage joint pain and inflammation. FlexPro MD

Topics: Animals; Arthralgia; Euphausiacea; Humans; Hyaluronic Acid; Osteoarthritis

Chondrocyte degeneration and classically activated macrophage (AM)-related inflammation play critical roles in osteoarthritis (OA). Here, we explored the effects of astaxanthin and Rspo2 on OA

Topics: beta Catenin; Cells, Cultured; Chondrocytes; Humans; Macrophages; Osteoarthritis; Wnt Signaling Pathway

Ferroptosis is a novel form of regulated cell death that has a close association with mitochondrial dysfunction and is characterized by iron overload, the accumulation of reactive oxygen species (ROS), and lipid ROS. Chondrocytes ferroptosis accelerates the progression of osteoarthritis (OA). Astaxanthin (ATX) is a xanthophyll carotenoid that possesses anti-inflammatory and antioxidant properties and has been explored in research studies for the treatment of diabetes and cardiovascular disease. However, the role it plays in OA, particularly in chondrocyte ferroptosis, has not yet been reported. In this study, ferroptosis-related events were analyzed in rat chondrocytes in vitro. A surgical destabilized medial meniscus was performed for the establishment of in vivo OA model. The results showed that interleukin-1β (IL-1β) induced inflammatory injury in chondrocytes through the promotion of the expressions of inflammatory factors including inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX2). IL-1β triggered chondrocyte ferroptosis by increasing the levels of intracellular ROS, lipid ROS, iron, and mitochondrial iron and inhibiting the expressions of SLC7A11/glutathione peroxidase 4 (GPX4) and Ferritin. The above indices were ameliorated by ferrostatin-1 (Fer-1, a classic ferroptosis inhibitor) and ATX. Furthermore, Fer-1 and ATX rescued the IL-1β-induced down-regulating collagen type II (collagen Ⅱ) and up-regulating matrix metalloproteinase 13 (MMP13). Following treatment with IL-1β, mitochondrial membrane potential decreased and the mitochondrial membrane was broken. At the same time, the mitochondrion shrank, becoming deformed as the mitochondrial cristae reduced and became disrupted. These changes were entirely consistent with ferroptosis features. All the aforementioned phenomena were reversed by Fer-1 and ATX. In addition, intra-articular injection of Fer-1 and ATX delayed articular cartilage degradation and OA progression. This study demonstrated that IL-1β can induce inflammatory damage and ferroptosis in chondrocytes. Both Fer-1 and ATX have the ability to mitigate chondrocyte injury and osteoarthritis progression by inhibiting ferroptosis and the regulation of mitochondrial function. Targeting ferroptosis has the potential to be a promising future treatment method for OA.

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Cells, Cultured; Chondrocytes; Collagen Type II; Cyclooxygenase 2; Ferritins; Ferroptosis; Interleukin-1beta; Iron; Lipids; Matrix Metalloproteinase 13; Mitochondria; Nitric Oxide Synthase Type II; Osteoarthritis; Phospholipid Hydroperoxide Glutathione Peroxidase; Rats; Reactive Oxygen Species; Xanthophylls

Osteoarthritis (OA) is a degenerative joint disease and a leading cause of adult disability. Since there is no cure for OA and no effective treatment to slow its progression, current pharmacologic treatments, such as analgesics and non-steroidal anti-inflammatory drugs (NSAIDs), only alleviate symptoms, such as pain and inflammation, but do not inhibit the disease process. Moreover, chronic intake of these drugs may result in severe adverse effects. For these reasons, patients have turned to the use of various complementary and alternative approaches, including diverse dietary supplements and nutraceuticals, in an effort to improve symptoms and manage or slow disease progression. The present study was conducted to evaluate the anti-osteoarthritic effects of FlexPro MD

Topics: Animals; Cartilage, Articular; Dietary Supplements; Disease Models, Animal; Euphausiacea; Hyaluronic Acid; Inflammation; Iodoacetates; Male; Osteoarthritis; Pain; Phytotherapy; Plant Oils; Rats, Sprague-Dawley; Treatment Outcome; Xanthophylls

Osteoarthritis (OA) is a progressive disease characterized by cartilage degradation. Astaxanthin (Ast), a natural compound with remarkable antioxidant activity and multiple medical applications due to its activation of Nrf2 signaling, has been studied for application to various degenerative diseases. Currently, however, little is known about its efficacy in treating OA. This study reports the effects of Ast on cartilage homeostasis in OA progression.. IL-1β, TNF-α, and tert-butyl hydroperoxide (TBHP) were used to impair cartilage homeostasis. Modulating effects of Ast on the Nrf2 signaling pathway, and damage-associated events including extracellular matrix (ECM) degradation, inflammation, oxidative stress, chondrocyte apoptosis, and. Ast attenuated ECM degradation of OA chondrocytes through the Nrf2 signaling, and ameliorated the IL-1β-induced inflammatory response and ECM degradation via blockade of MAPK signaling. Additionally, Ast alleviated TNF-α-induced ECM degradation and chondrocyte apoptosis by inhibiting the NF-κB signaling, suppressed TBHP-induced oxidative stress, and subsequently reduced chondrocyte apoptosis.. Ast could protect against osteoarthritis via the Nrf2 signaling, suggesting Ast might be a potential therapeutic supplement for OA treatment.

Topics: Animals; Cartilage, Articular; Chondrocytes; Homeostasis; Male; Mice; Mice, Inbred C57BL; NF-E2-Related Factor 2; Osteoarthritis; Xanthophylls

Astaxanthin is a red-pigment carotenoid found in certain marine animals and plants. Astaxanthin has been shown to inhibit matrix metalloproteinases (MMPs) expression in vitro. However, the effect of astaxanthin on cartilage is still unclear. The aim of this study was to investigate the effects of astaxanthin on cartilage in experimental osteoarthritis (OA).. New Zealand rabbits underwent anterior cruciate ligament transection to induce OA in right knee. Rabbits received intra-articular injection containing 0.3 ml of vehicle (dimethyl sulfoxide) or astaxanthin (50 μM). Injection was started on the day of operation, and the injection were performed once weekly for six consecutive weeks. Then, rabbits were sacrificed and the right knees were harvested for study.. Cartilage degradation was reduced by astaxanthin, as assessed by morphological and histological examination. Astaxanthin inhibited the gene expression of MMP-1, MMP-3, and MMP-13 in cartilage as compared with the vehicle group.. The results suggest that astaxanthin may be considered as pharmaceutical agent in OA treatment.

Topics: Animals; Arthritis, Experimental; Cartilage, Articular; Fibrinolytic Agents; Injections, Intra-Articular; Osteoarthritis; Rabbits; Xanthophylls