Abstract
Objective: The objective of the present study is to evaluate the effect of Phthalate analogues of diclofenac in Freund’s complete adjuvant (FCA) induced Arthritis in the rat.
 Methods: Twenty four female albino wistar rats were enrolled in this study and are divided into 4 groups (six each). The groups were designed as follows: Group I: vehicle control, Group II: arthritic control, Group III: diclofenac treated, Group IV: phthalate analogue of diclofenac treated. Various assessments such as anti-arthritic activity, biochemical estimations, haematological parameters, ulcerogenesis, radiological and histopathological studies were evaluated.
 Results: Arthritic control group exhibited significant increase in the level of paw volume, arthritic score (p<0.0001), Serum glutamic pyruvic transaminase (SGPT) (p<0.001), Serum glutamic oxaloacetic transaminase (SGOT) p<0.01), rheumatoid arthritis factor, C-reactive protein (CRP), White Blood Cells (WBC), Creatinine and uric acid and a significant decrease in Red Blood Cells (RBC). Increased swelling of joints, bony destruction and profound ulceration were observed in the Arthritic control group. All these conditions were reversed in diclofenac and phthalate analogue of diclofenac groups.
 Conclusion: We conclude that phthalate analogue of diclofenac shows potent anti-arthritic activity with milder ulceration when compared to diclofenac treatment.
Highlights
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease with the main clinical manifestation of systemic complications including synovial inflammation, joint lesion and bone damage [1]
Rheumatoid arthritis is characterized by the presence of autoantibodies known as rheumatoid factors (RF) and anti-citrullinated peptide antibodies (ACPA)
Effect of phthalate analogue of diclofenac changes in acute oral toxicity studies The phthalate analogue of diclofenac does not produce any toxic symptoms or mortality up to dose level of 300 mg/kg orally in mice and the drug was considered safe for further pharmacological screening
Summary
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease with the main clinical manifestation of systemic complications including synovial inflammation, joint lesion and bone damage [1]. In RA, pannus is rich in secretion of activated macrophages and other inflammatory mediators, resulting in the destruction of tissues when compared to normal synovial fluid, which is essentially a cellular [2]. Rheumatoid arthritis is characterized by the presence of autoantibodies known as rheumatoid factors (RF) and anti-citrullinated peptide antibodies (ACPA). RA synovial fluid is abundant in neutrophils, macrophages, T lymphocytes, autoantibodies and dendritic cells. Chondrocytes secrete proteolytic enzymes that lead to destruction of articular cartilage causing bone deformity and loss of joint function. It is thought that costimulation of both humoral and cellular immunity may contribute to the pathology of the disease [5]
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