Abstract
Objective This study aims to evaluate the efficacy of moxibustion on joint swelling and pain and the levels of C-X-C motif chemokine ligand 1 (CXCL1), β-endorphin (β-EP) in serum of rheumatoid arthritis (RA) patients and to investigate the anti-inflammatory and analgesic mechanism of moxibustion on improving RA. Methods Sixty-eight patients with RA were randomly and equally classified into the control and treatment groups. The control group was treated with routine drug therapy, while the treatment group received routine drug therapy and moxibustion. Both groups were treated for eight weeks. The symptoms and laboratory indicators of RA patients were compared in the two groups before and after intervention. Results Sixty-one patients completed the study: four patients dropped out from the treatment group and three from the control group. Trial endpoints were change (∆) in symptoms, measured by Ritchie's articular index (RAI), swollen joint count (SJC), and laboratory indicators, measured by the level of CXCL1, β-EP, tumor necrosis factor-a (TNF-α), and interleukin-1β (IL-1β). ∆RAI, ∆SJC, ∆CXCL1, ∆β-EP, ∆TNF-α, and ∆IL-1β in the treatment group were superior to the control group (13.50 [14.50] versus 6.00 [13.00] in ∆RAI, 4.00 [3.00] versus 2.00 [4.00] in ∆SJC, 0.04 ± 0.79 ng/mL versus -0.01 ± 0.86 ng/mL in ∆CXCL1, -2.43 [5.52] pg/mg versus -0.04 [4.09] pg/mg in ∆β-EP, 3.45 [5.90] pg/mL versus 1.55 [8.29] pg/mL in ∆TNF-α, and 6.15 ± 8.65 pg/mL versus 1.28 ± 8.51 pg/mL in ∆IL-1β; all P < 0.05). Conclusion Moxibustion can improve the joint swelling and pain symptoms in patients with RA, which may be related to the fact that moxibustion can reduce the release of inflammatory factors in patients with RA and downregulate the level of CXCL1 and increase the level of β-EP at the same time. This trial is registered with ChiCTR-IOR-17012282.
Highlights
Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease characterized by pain, stiffness, swelling, and tenderness of synovial joints, resulting in joint destruction, disability, and decline in quality of life [1]. e global incidence of RA is about 0.5–1.0% [2], and the incidence in China is about 0.5% [3]. e lifetime prevalence rate is as high as 1% in the world. e course of RA can be as long as several decades
A total of 61 patients completed the study, with four patients dropped from the treatment group and three from the control group (Figure 1). ere were a total of 30 patients in the treatment group, including four males and 26 females, with an average age of 53.0 ± 8.80 years and an average course of disease of 10.11 ± 9.02 years. ere were 31 patients in the control group, including five males and 26 females, with an average age of 49.39 ± 7.72 years and an average course of disease of 9.13 ± 9.09 years. ere was no significant difference in general information between the two groups (P > 0.05), and the baseline was balanced and comparable
Trial main endpoints were improved in symptoms, measured by the Ritchie’s articular index [23] (RAI indicates the degree of joint pain), and the swollen joint count (SJC) and laboratory indicators, measured by the level of CXCL1, β-EP, TNF-α, and IL-1β in serum
Summary
Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease characterized by pain, stiffness, swelling, and tenderness of synovial joints, resulting in joint destruction, disability, and decline in quality of life [1]. e global incidence of RA is about 0.5–1.0% [2], and the incidence in China is about 0.5% [3]. e lifetime prevalence rate is as high as 1% in the world. e course of RA can be as long as several decades. Cytokines released by inflammatory cells in joints, such as tumor necrosis factor superfamily, interferon, interleukin, and chemokines, are all important pain-causing substances that promote continuous joint inflammatory response and hyperalgesia in RA patients [5,6,7]. C-X-C motif chemokine ligand 1 (CXCL1) is one of the chemokines secreted by fibroblasts in synovium mediated by tumor necrosis factor-a (TNF-α) and interleukin-1β (IL-1β). It can promote inflammatory response [9], promote angiogenesis [8], and enhance the sensitivity and excitability of peripheral sensory neurons [10, 11]. It is important to note that inflammation plays a painful role and triggers immune cells containing opioid peptides to gather and release endogenous opioid peptide at the inflammatory site, resulting in an analgesic effect [12,13,14]. β-endorphin (β-EP), as an endogenous opioid peptide with typical opioid like effects, acts on opioid receptors on primary afferent neurons through secretion of immune cells, blocking pain transmission, so as to achieve analgesic effect [15], and regulates immune function by binding to receptors on immune cells [16, 17]. erefore, the changes of chemokines and endogenous opioid peptides in vivo are closely related to the disease development and clinical symptoms of RA patients
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