Abstract
Background Moxibustion has a therapeutic effect of reducing swelling and relieving pain in patients with rheumatoid arthritis (RA) but its mechanism is uncertain. Objective To evaluate the effect of moxibustion on serum levels of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) in patients with RA and to explore the possible mechanism of moxibustion. Methods This study involved 46 RA patients who had fulfilled the inclusion criteria and were randomly assigned to a treatment group and a control group in an equal ratio. The control group was treated with methotrexate or leflunomide, while the treatment group received methotrexate or leflunomide and moxibustion at ST 36 (Zusanli), BL 23 (Shenshu), and Ashi points. Patients' clinical symptoms, RA-associated serum markers, and serum levels of TNF-α, IL-1β, HIF-1α, and VEGF were compared in the two groups before and after intervention. Statistical analysis was performed using SPSS 21.0 statistical software. Results 37 of 46 RA patients eventually completed the whole treatment course. Compared with the control group, the treatment group significantly improved the clinical symptoms (P < 0.05) but with no significant differences in RA-associated serum markers (P > 0.05). There were significant differences in TNF-α and IL-1β among the groups after 8 weeks of treatment (P < 0.05). HIF-1α and VEGF were decreased in the treatment group after therapy (P < 0.05). VEGF was reduced in the control group (P < 0.05), while HIF-1α was not significantly improved (P > 0.05). The reductions of HIF-1α and VEGF in the treatment group were superior to the control group (P < 0.05). Conclusions Moxibustion enhanced the anti-inflammatory and analgesic effects of conventional medicine and can enhance the effect of conventional medicine, downregulating HIF-1α/VEGF contents to inhibit angiogenesis.
Highlights
Rheumatoid arthritis (RA) is a chronic inflammatory joint disease, which can cause cartilage and bone damage as well as disability [1]. e morbidity of RA is as high as 0.18–1.07%all over the world, which shows an increasing trend year by year [2].e basic pathogenesis of RA is generally centered around the underlying inflammatory process that affects the synovium of the joint which is commonly associated with angiogenesis, Pain Research and Management the formation of new blood vessels from the pre-existing vascular network [3, 4]
Hypoxia-inducible factor (HIF) -1α, which abundantly expressed under micro-oxygen conditions, contributes to hypoxia-augmented inflammatory cytokine production, promotes angiogenesis, invasion, and metastasis, and with the addition of proinflammatory cytokines TNF-α and IL-1β up-regulates the expression of vascular endothelial growth factor (VEGF) under hypoxia to promote angiogenesis [11, 12]. erefore, hypoxia-inducible factor-1α (HIF-1α) and VEGF levels in RA patients can reflect the progression of angiogenesis from one aspect
We found the contents of HIF-1α and VEGF can be regulated by moxibustion ST 36 and BL 23 to inhibit the formation of blood vessels in RA rabbit synovial tissue. erefore, the aim of this study was to discuss the effect of moxibustion on the levels of angiogenesis-related factors HIF-1α and VEGF in RA patients, which can provide a more solid basis for moxibustion in RA treatment
Summary
E basic pathogenesis of RA is generally centered around the underlying inflammatory process that affects the synovium of the joint which is commonly associated with angiogenesis, Pain Research and Management the formation of new blood vessels from the pre-existing vascular network [3, 4]. Erefore, HIF-1α and VEGF levels in RA patients can reflect the progression of angiogenesis from one aspect. To evaluate the effect of moxibustion on serum levels of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) in patients with RA and to explore the possible mechanism of moxibustion. E reductions of HIF-1α and VEGF in the treatment group were superior to the control group (P < 0.05). Moxibustion enhanced the antiinflammatory and analgesic effects of conventional medicine and can enhance the effect of conventional medicine, downregulating HIF-1α/VEGF contents to inhibit angiogenesis
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