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Osteoarthritis (OA) is a degenerative disorder involving the joint, including cartilage and synovial fluids. Recent studies have sought to find curative therapeutics to decrease the adverse effects of OA and relieve associated pain. Globally, knee osteoarthritis (KOA) is the most common type of arthritis. The present study aimed to evaluate the anti-inflammatory effect copper albumen complex (cu-albumin complex) for the treatment of mono-iodoacetate (MIA)- induced KOA in Albino rats. A total of 50 adult male albino rats were involved and divided as follows; 10 rats were kept normal as negative control; 20 arthritic rats were kept untreated (positive control), and 20 arthritic rats were treated with cu-albumin complex orally for a month. Treated and untreated arthritic rats were divided equally (10 rats each) into mild and severe groups according to the severity of signs. The intra-articular injection of MIA in the right knee joint was used for induction of osteoarthritis. Using Mankin grading score, the results demonstrated that the treated groups had a better histological appearance than the control positive group. Additionally, except for a few shrunken chondrocytes, the mildly treated group showed less degenerative alterations and appeared virtually normal. While the severe treated group showed increased cellularity with decreased degenerated chondrocytes. It concluded that balanced copper consumption has a positive impact on the prevention and treatment of KOA

Nitrosodiethylamine (NDEA) is a potent oxidant induces neurodegeneration via (reactive oxygen species) ROS. Copper is an important metal essential for scavenging free radicals, development of central nervous system (CNS) and redox angiogenesis signaling. Vascular endothelial growth factor (VEGF) is well known as efficacious and long-term signal that stimulates angiogenesis, where its expression is copper dependent. We examined the copper protective effect against brain vascular damage initiated by NDEA. NDEA induces brain vascular wall damage, necrosis with interstitial hemorrhage and diminishes VEGF expression. Histopathological examination showing a great improvement of brain tissue in copper treated mice with significant increase in VEGF expression. Higher levels of intracellular copper can stimulate angiogenesis and exhibited a significant protection against NDEA induced brain vascular damage, confirming its ability to enhance antioxidant activity and angiogenesis initiation. Our report presents first evidence that inducible VEGF expression in brain is sensitive to copper; moreover, copper-based therapeutics represents a novel approach to reduce brain vascular damage induced by NDEA generated ROS