Abstract

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.

Keywords: Aggrcan, Copper, Knee, MIA, Osteoarthritis, Proteoglycan.

Retinitis pigmentosa (RP) affects over a million people worldwide, characterized by photoreceptor cell death, progressive retinal degeneration, and visual loss. Metformin is demonstrated as a potential therapeutic approach for preventing light-induced retinal degeneration by decreasing apoptosis and oxidative stress. This work aimed to investigate the effect of metformin on the retina of the N-Ethyl-N-nitrosourea (ENU) induced rat model of RP. Eighteen adult male Wistar rats were divided into two groups. Group I: normal vehicle control (N = 6). Group II: ENU-induced photoreceptor degeneration (N = 12) received a single intraperitoneal injection of ENU at a 600 mg/kg dose. Rats in group II were equally divided into two subgroups: IIa: photoreceptor degeneration-induced group and IIb: metformin-treated group (200 mg/kg) for seven days. Specimens from the retina were processed for light and electron microscopy …

الوصف

Acquired or inherited or photoreceptor loss causes retinal ganglion cell loss and ultimately axonal transport alteration. Thus, therapies should be applied early during photoreceptors degeneration before the remodeling process reaches the inner retina. This study aimed to evaluate the protective effect of metformin on the rat optic nerve following photoreceptors loss induced by N-Ethyl-N-nitrosourea (ENU). Eighteen adults male Wistar rats were divided into two groups. Group I: normal vehicle control (n= 6). Group II: ENU-induced photoreceptors degeneration (n= 12) received a single intraperitoneal injection of ENU at a dose of 600 mg/kg. Rats in group II were equally divided into two subgroups: IIa: photoreceptor degeneration induced group and IIb: metformin treated group (200 mg/kg) for 7 days. Specimens from the optic nerve were processed for light and electron microscopy. In ENU treated group, the optic nerve revealed reduction in the diameter of the optic nerve fibers and thinning of myelin sheath with morphological changes in the glia (astrocytes, oligodendrocytes, and microglia). Caspase-3 (apoptotic marker), iNOS (oxidative stress marker) and CD68 (macrophage marker) expression increased. In metformin-treated group, the diameter of optic nerve fibers and myelin sheath thickness increased with improvement of the deterioration in the glia. Caspase-3, iNOS and CD68 expression decreased. Metformin ameliorates the histological changes of the rat optic nerve following photoreceptors loss induced by ENU.