Research Article: The clinical efficacy and mechanism of Rhodiola rosea in treating rheumatoid arthritis in high-altitude areas by regulating the HIF-1? signaling pathway
Abstract:
To evaluate the clinical efficacy of Rhodiola rosea in high-altitude rheumatoid arthritis (RA) patients and to investigate, in vitro , whether its anti-inflammatory mechanism is mediated by the HIF-1? signaling pathway.
This study adopted a retrospective analysis. Patients with RA in high-altitude areas were divided into the Rhodiola rosea treatment group (74 cases) and the conventional treatment group (86 cases). Baseline data, disease activity score (DAS28), inflammatory factors (CRP, ESR, TNF- ? , and IL-6), serum HIF-1? levels, imaging data, and adverse reaction monitoring data were collected to evaluate the clinical efficacy and safety of Rhodiola rosea. Human synovial cells (HFLS-RA) were used for in vitro experiments to establish a hypoxic model. Using CCK-8, qRT-PCR, Western Blot, and gene overexpression techniques, the molecular mechanism was further explored.
The Rhodiola rosea treatment group showed significantly better improvements in DAS28, CRP, ESR, TNF- ? , and IL-6 compared to the conventional treatment group ( p <?0.05). Imaging assessment showed greater reductions in synovial thickness and blood-flow signals in the knee and metacarpophalangeal joints in the Rhodiola rosea group than in the conventional treatment group. The serum HIF-1? level in the Rhodiola rosea group was significantly lower, and the incidence of adverse reactions (18.92%) was significantly lower than that of the conventional treatment group (34.88%), without any serious adverse events. The in vitro experiments showed that Rhodiola rosea injection (RRI) reduced hypoxia-induced expression of HIF-1? and its downstream factors MMP-3, VEGF, COX-2, and ICAM-1.
Rhodiola rosea was associated with improved disease activity and inflammatory markers in high-altitude RA patients, with a favorable safety profile. The in vitro findings suggest that inhibition of HIF-1? signaling may be one potential mechanism, although prospective and translational validation is still required.
Introduction:
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation, joint destruction, and systemic complications ( 1–3 ). Its pathogenesis involves immune dysregulation and excessive pro-inflammatory cytokines ( 4 , 5 ). Epidemiological studies show that in high-altitude regions, chronic hypoxic exposure exacerbates synovial inflammation, tissue damage, and therapeutic resistance ( 6 , 7 ), highlighting the need for region-specific treatment strategies. Hypoxia is a key driver of RA…
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