Inflammation in the Pathogenesis of Rheumatoid Arthritis and in Experimental Arthritis: Evaluation of Combinations of Carnosic Acid and Extract of Rhodiola rosea L. with Methotrexate

S. Poništ, K. Pružinská, K. Bauerová
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引用次数: 1

Abstract

The host immune response generates the pro-inflammatory immune response as a protective measure against invading pathogens, allergens, and/or trauma. However, dysregulated and chronic inflammation may result in secondary damage to tissues and immune pathology to the host. Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease which primarily involves synovial inflammation, joint pain, immobility, and stiffness. Increased infiltration of inflammatory immune cells and fibroblast-like synoviocytes into joints, form pannus and small blood vessels that lead to synovium and cartilage destruction. In this chapter we will focus on the role of inflammatory cytokines (IL-1β, IL-6 and IL-17), chemokine monocyte chemotactic protein-1 and matrix metalloproteinase-9 in the pathogenesis of experimental arthritis in animals and in human RA. Further, we will be discussing about methotrexate’s (cornerstone of anti-rheumatic therapy) immune suppressing activity, anti-inflammatory properties of carnosic acid and extract of Rhodiola rosea L., and their innovative combination treatments with methotrexate in rat adjuvant arthritis.
类风湿关节炎发病机制中的炎症及实验性关节炎:鼠尾草酸、红景天提取物与甲氨蝶呤联合应用的评价
宿主免疫反应产生促炎免疫反应,作为对入侵病原体、过敏原和/或创伤的保护措施。然而,失调和慢性炎症可能导致组织的继发性损伤和宿主的免疫病理。类风湿性关节炎(RA)是一种慢性系统性自身免疫性疾病,主要涉及滑膜炎症、关节疼痛、不活动和僵硬。炎性免疫细胞和成纤维细胞样滑膜细胞向关节的浸润增加,形成滑膜和小血管,导致滑膜和软骨破坏。在本章中,我们将重点关注炎症因子(IL-1β, IL-6和IL-17),趋化因子单核细胞趋化蛋白-1和基质金属蛋白酶-9在动物和人类RA的实验性关节炎发病机制中的作用。此外,我们将讨论甲氨蝶呤(抗风湿病治疗的基石)的免疫抑制活性,鼠尾草酸和红景天提取物的抗炎特性,以及它们与甲氨蝶呤在大鼠佐剂性关节炎中的创新联合治疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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