Abstract
In this study, we attempted to identify and assess effects of isoegomaketone (IK) isolated from Perilla frutescens var. crispa on the development of rheumatoid arthritis (RA). RA was induced in male Balb/c mice by collagen antibody injection. Experimental animals were randomly divided into five groups: normal, collagen antibody-induced arthritis (CAIA), CAIA + IK (5 mg/kg/day), CAIA + IK (10 mg/kg/day), and CAIA + apigenin (16 mg/kg/day) and respective treatments were administered via oral gavage once per day for four days. Mice treated with IK (10 mg/kg/day) developed less severe arthritis than the control CAIA mice. Arthritic score, paw volume, and paw thickness were less significant compared to the control CAIA mice at day seven (73%, 15%, and 14% lower, respectively). Furthermore, histopathological examination of ankle for inflammation showed that infiltration of inflammatory cells and edema formation were reduced by IK treatment. Similarly, neutrophil to lymphocyte ratio (NLR) in whole blood was lower in mice treated with IK (10 mg/kg/day) by 85% when compared to CAIA mice. Taken together, treatment with IK delays the onset of the arthritis and alleviates the manifestations of arthritis in CAIA mice.
Highlights
Rheumatoid arthritis (RA) is a systemic autoimmune disease in which chronic joint inflammation leads to cartilage destruction and bone erosion [1]
The use of standard drugs in RA is known to produce a variety of side effects: Infusion hypersensitivity reactions with the use of TNF-α inhibitors [5]; gastrointestinal ulcerations and hemorrhagic events triggered by NSAID [6]; higher risk of infection due to the use of biological drugs [7]; etc
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Summary
Rheumatoid arthritis (RA) is a systemic autoimmune disease in which chronic joint inflammation leads to cartilage destruction and bone erosion [1]. About 1% of US population is affected by RA, and RA increases the risk for cardiovascular disease, lymphoma, and death [2]. RA is treated with steroidal/nonsteroidal anti-inflammatory drugs (NSAID) or biological modulators such as tumor necrosis factor alpha (TNF-α) inhibitors and interleutkin-1 (IL-1) receptor antagonists [3]. Acetaminophen, a kind of NSAID, is most frequently implemented and taken in very high doses (4 g/day) [4]. The use of standard drugs in RA is known to produce a variety of side effects: Infusion hypersensitivity reactions with the use of TNF-α inhibitors [5]; gastrointestinal ulcerations and hemorrhagic events triggered by NSAID [6]; higher risk of infection due to the use of biological drugs [7]; etc. The need for new cure in RA is still high
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