Abstract
Purpose: To investigate the anti-arthritic activity of arglabin in Freund’s complete adjuvant- induced arthritis in rats, and the likely underlying mechanism.Methods: A total of 40 male albino Wistar rats weighing between 120 and 150 g were used for this study. The rats were divided into four groups of ten rats each: control group, arthritis group, arglabintreated group, and standard (STD) group. Chronic arthritis was induced by injecting Freund's complete adjuvant in the plantar region of the rats. Rats in the arglabin-treated group received 5 ng/g arglabin intraperitoneally (i.p.), while those in the STD group received 1.5 mg/kg indomethacin, p.o. for 4 weeks. The development of arthritis was assessed at 0, 7, 14, 21 and 28th day of protocol by measuring thermal hyperalgesia, mechanical nociceptive threshold, arthritic score and paw volume. Activities of liver alkaline phosphatase (ALP), alanine amino-transaminase (ALT) and aspartate amino-transaminase (AST), and the levels of inflammatory cytokines -tumor necrosis factor-α (TNF-α), interferon gamma (IFN-γ), interleukin (IL)-6 and interleukin (IL)-1β were measured in the synovial fluid, while those of inflammatory mediators - thromboxane B2 (TXB2), prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) were determined in serum. The expressions of mRNAs of nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB), cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were also determined in rat synovial tissues.Results: Arglabin significantly decreased the paw swelling and arthritic scores, but significantly increased the paw withdrawal latency, when compared to the arthritis group (p < 0.05). It also attenuated the altered levels of inflammatory cytokines in arthritic rats, and significantly reduced the levels of inflammatory mediators, when compared to the arthritis group (p < 0.05). The expressions of mRNAs of NFkB, COX-2 and iNOS also significantly decreased in arglabin-treated group, relative to the arthritis group (p < 0.05).Conclusion: The anti-arthritic activity of arglabin is due to its effect on inflammatory pathway via decreases in the levels of inflammatory mediators and cytokines, and decrease in the expressions of NFkB, COX-2 and iNOS in the synovial tissues of arthritic rats.Keywords: Arglabin, Arthritis, Freund’s complete adjuvant, Inflammatory cytokines
Highlights
Arthritis is an inflammatory disorder of the joints which affects approximately 10 % of the world’s population [1]
Studies have revealed that inflammatory cytokines play important role in the pathogenesis of rheumatoid arthritis (RA) and OA [6], which are conventionally managed with non- steroidal antiinflammatory drugs (NSAIDs) and analgesics
Arthritis was induced in the rats by a single injection of Freund’s complete adjuvant and they were treated with arglabin for a period of four weeks
Summary
Arthritis is an inflammatory disorder of the joints which affects approximately 10 % of the world’s population [1]. Osteoarthritis affects approximately 3.6 % of the world’s population [5], and it is an inflammatory disorder of joints characterised by joint pain, cartilage damage and development of osteophytes. A sesquiterpene gamma-lactone isolated from different plant species such as Artemisia glabella, has tremendous pharmacological potential [7,8]. It possesses antimicrobial, antiinflammatory, neuroprotective and anticancer activities [9,10,11]. The aim of this study was to investigate the anti-arthritic activity of arglabin in Freund’s complete adjuvantinduced arthritis in rats, and to identify the likely mechanism involved
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