Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Arglabin as a potential drug in the treatment of Freund's complete adjuvant-induced arthritis in rats

Xiangchun Liu¹ , Heng Jia², Hongsheng Xia³

¹Department of Orthopedics, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100035; ²Department of Joint Surgery, Chinese Medicine Hospital of the Xinjiang Uygur Autonomous Region, Urumqi, 830000; ³Department of Orthopedics, Huguosi Hospital, Beijing University of Chinese Medicine, Beijing 100035, China.

For correspondence:- Xiangchun Liu Email: xiangchunliu43@hotmail.com Tel:+861084013276

Accepted: 27 July 2018 Published: 31 August 2018

Citation: Liu X, Jia H, Xia H. Arglabin as a potential drug in the treatment of Freund's complete adjuvant-induced arthritis in rats. Trop J Pharm Res 2018; 17(8):1585-1590 doi: 10.4314/tjpr.v17i8.17

© 2018 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

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, arglabin-treated 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 (NF_kB), 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 NF_kB, 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 NF_kB, COX-2 and iNOS in the synovial tissues of arthritic rats.

Keywords: Arglabin, Arthritis, Freundâ€™s complete adjuvant, Inflammatory cytokines