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Salvia plebeia extract inhibits the inflammatory response in human rheumatoid synovial fibroblasts and a murine model of arthritis
Institution:1. CMRI, Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 700-422, Republic of Korea;2. Bio-Materials Research Institute, Korea Research Institute of Bioscience and Biotechnology, Jeongeup 580-185, Republic of Korea;3. R&D Center Pharmaceutical lab, Korean Drug Co., LTD, Seoul 135-270, Republic of Korea;4. Department of Internal Medicine (Rheumatology), School of Medicine, Kyungpook National University, Daegu 700-422, Republic of Korea;5. College of Pharmacy, Yeungnam University, Gyeongbuk 712-749, Republic of Korea;6. College of Pharmacy, Woosuk University, Jeonju 565-701, Republic of Korea;1. Department of Biochemistry and Molecular Biology, University of Las Palmas de Gran Canaria, Plaza Dr. Pasteur s/n, 35016 Las Palmas de Gran Canaria, Spain;2. Department of Chemistry, University of Las Palmas de Gran Canaria, Campus de Tafira, 35017 Las Palmas de Gran Canaria, Spain;1. Medicines Authority, 203 Level 3, Rue D''Argens, Gzira, GZR 1368, Malta;2. Institute of Earth Systems, University of Malta, Malta;3. Department of Pharmacy, Faculty of Medicine and Surgery, University of Malta, Msida, Malta;4. Department of Biology, School of Pharmacy, University of Tor Vergata, Rome, Italy;1. Institute of Materia Medica, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing 100050, China;2. Pharmacy Department of the Affiliated Hospital of Qingdao University, Qingdao 266003, China;3. Binzhou Medical University, Yantai 264003, China
Abstract:Salvia plebeia R. Br. has been used to treat a variety of inflammatory diseases and as an antioxidant in many countries, including Korea and China. In this study, we investigated the effects of S. plebeia extract (SPE) on inflammatory arthritis and the underlying mechanisms of action. We used a collagen-induced arthritis (CIA) mouse model. TNF-α-stimulated rheumatoid arthritis (RA) synovial fibroblasts were used to elucidate the underlying mechanisms of action. Oral administration of SPE improved the clinical arthritis score, footpad thickness, and histologic changes, as well as serum IgG1 and IgG2a levels. SPE administration inhibited Th1/Th2/Th17 phenotype CD4+ T lymphocyte expansion in inguinal lymph node and expression of inflammatory mediators such as cytokines, MMP-1, and MMP-3 in the ankle joint tissue. SPE significantly suppressed the expression of cytokines and MMP-1 by down-regulating NF-κB, Akt, and mitogen-activated protein kinases in RA synovial fibroblasts. Taken together, these results indicate that SPE is therapeutically efficacious against chronic inflammatory arthritis, suggesting that SPE is a candidate for treating RA.
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