Abstract
Physical exercise (PE) is recommended for Rheumatoid Arthritis (RA), but the molecular and biological mechanisms that impact the inflammatory process and joint destruction in RA remain unknown. The objective of this study was to evaluate the effect of PE on the histological and transcriptional changes in the joints of adjuvant-induced arthritis (AIA) rat model. AIA rats were subjected to PE on a treadmill for eight weeks. The joints were subjected to histological and microarray analysis. The differentially expressed genes (DEGs) by PE in the arthritic rats were obtained from the microarray. The bioinformatic analysis allowed the association of these genes in biological processes and signaling pathways. PE induced the differential expression of 719 genes. The DEGs were significantly associated with pathogenic mechanisms in RA, including HIF-1, VEGF, PI3-Akt, and Jak-STAT signaling pathways, as well as response to oxidative stress and inflammatory response. At a histological level, PE exacerbated joint inflammatory infiltrate and tissue destruction. The PE exacerbated the stressed joint environment aggravating the inflammatory process, the hypoxia, and the oxidative stress, conditions described as detrimental in the RA joints. Research on the effect of PE on the pathogenesis process of RA is still necessary for animal models and human.
Highlights
Rheumatoid arthritis (RA) is one of the most common inflammatory arthritis affecting 0.5–1.0%of the population [1]
The maximal physical capacity obtained in the physical capacity test (PCT) for the arthritis-exercise group was 21.28 ± 5.96 m/min
The present study explored the influence of Physical exercise (PE) in the genetic expression and the histology of the actively swollen joints in the adjuvant-induced arthritis (AIA) model
Summary
Rheumatoid arthritis (RA) is one of the most common inflammatory arthritis affecting 0.5–1.0%of the population [1]. Rheumatoid arthritis (RA) is one of the most common inflammatory arthritis affecting 0.5–1.0%. RA is a systemic autoimmune disease characterized by inflammation of the synovial membrane and periarticular structures. Extra-articular manifestations, including cardiovascular, pulmonary, psychological and skeletal disorders are common in RA patients [2]. The etiology and pathophysiology of RA remain unresolved; genetic and environmental factors have been associated with the inappropriate immunomodulation that triggers the inflammatory process in the joints and the subsequent damage to synovial structures [3]. The treatment of RA aims to reduce pain and inflammation in the joints and to preserve their structural integrity and the patient’s functionality. Treatment includes a variety of pharmacological agents, education programs, joint protection, lifestyle changes, PE and surgical intervention as a final step [4,5,6]
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