Anti-inflammatory and Anti-oxidant Properties of Curcuma longa (Turmeric) Versus Zingiber of ficinale (Ginger) Rhizomes in Rat Adjuvant-Induced Arthritis Gamal Ramadan, 1,2,3 Mohammed Ali Al-Kahtani, 1 and Wael Mohamed El-Sayed 1,2 Abstract—Turmeric (rich in curcuminoids) and ginger (rich in gingerols and shogaols) rhizomes have been widely used as dietary spices and to treat different diseases in Ayurveda/Chinese medi- cine since antiquity. Here, we compared the anti-inflammatory/anti-oxidant activity of these two plants in rat adjuvant-induced arthritis (AIA). Both plants (at dose 200 mg/kg body weight) signi- ficantly suppressed (but with different degrees) the incidence and severity of arthritis by increasing/ decreasing the production of anti-inflammatory/pro-inflammatory cytokines, respectively, and acti- vating the anti-oxidant defence system. The anti-arthritic activity of turmeric exceeded that of ginger and indomethacin (a non-steroidal anti-inflammatory drug), especially when the treatment started from the day of arthritis induction. The percentage of disease recovery was 4.6–8.3% and 10.2% more in turmeric compared with ginger and indomethacin (P <0.05), respectively. The present study proves the anti-inflammatory/anti-oxidant activity of turmeric over ginger and indomethacin, which may have beneficial effects against rheumatoid arthritis onset/progression as shown in AIA rat model. KEY WORDS: rat adjuvant-induced arthritis; anti-inflammatory/anti-oxidant activity; Curcuma longa; indom- ethacin; Zingiber officinale. INTRODUCTION Rheumatoid arthritis (RA) is a chronic inflamma- tory and destructive joint disease that affects 1% of the adult population worldwide [1]. It leads to significant disability and a consequent reduction in quality of life, which have a substantial socio-economic impact [2]. Tumour necrosis factor(TNF)-α, interleukin(IL)-1β and IL-6 are known to be the primary cytokines that mediate the marked destruction of cartilage/bone in arthritis, and have thus been investigated as important biological targets to develop drugs for the treatment of active RA [3, 4]. These pro-inflammatory cytokines induce fever, wasting, and a number of inflammatory events under- lying RA including leucocytes adhesion/recruitment, angiogenesis, and tissue destruction/fibrosis [5]. In addition, they trigger the synthesis of proteolytic enzymes such as matrix metalloproteinases (MMPs) and the formation of osteoclasts, which ultimately lead to the destruction of joints and the impairment of their function [6]. The free radicals especially reactive oxygen species (ROS) are also involved in the pathogenesis of RA and induce cartilage destruction through either a direct degradative effect on matrix components or an indirect action via activation of MMPs [7]. Rat adjuvant- induced arthritis (AIA) shares several features with human RA including weight loss, oxidative tissue damage and inflammatory infiltration of synovial mem- brane in association with joints swelling/destruction [5, 8]. In this model, arthritis develops within 14–18 days after adjuvant injection [5] through cell-mediated auto- immunity by structural mimicry between the mycobac- terium capsule and the cartilage proteoglycans [9]. 1 Biological Science Department, College of Science, King Faisal University, Al-Hufof, Kingdom of Saudi Arabia 2 Zoology Department, Faculty of Science, Ain Shams University, Abbasseya 11566, Cairo, Egypt 3 To whom correspondence should be addressed at Zoology Depart- ment, Faculty of Science, Ain Shams University, Abbasseya 11566, Cairo, Egypt. E-mail: gamal_ramadan@hotmail.com 0360-3997/11/0400-0291/0 # 2010 Springer Science+Business Media, LLC Inflammation, Vol. 34, No. 4, August 2011 ( # 2010) DOI: 10.1007/s10753-010-9278-0 291