Exercise Therapy Research in Ankylosing Spondylitis-Induced Back Pain: A Bibliometric Study (2004-2023).

BACKGROUND Ankylosing spondylitis (AS), a chronic inflammatory disease predominantly causing back pain, affects up to 0.5% of the global population, more commonly in males. Frequently undiagnosed in early stages, AS is often associated with comorbid depression and anxiety, imposing significant healthcare burdens. Despite available pharmaceutical treatments, exercise therapy (ET) has emerged as an effective, side-effect-free alternative, particularly for managing AS-induced back pain. This study aims to explore the research trends in ET for treating AS back pain from 2004-2023. MATERIAL AND METHODS A comprehensive analysis of 437 articles, sourced from the Science Citation Index-Expanded within the Web of Science Core Collection, was conducted using CiteSpace 6.2.R5. This study spanned from 2004 to October 15, 2023, examining publications, authors, institutions, and keywords to assess keyword co-occurrences, temporal progressions, and citation bursts. RESULTS Research interest in ET for AS began escalating around 2008 and has since shown steady growth. The USA emerged as a significant contributor, with Van der Heijde, Desiree, and RUDWALEIT M being notable authors. Key institutions include Assistance Publique Hopitaux Paris and UDICE-French Research Universities, with ANN RHEUM DIS being the most influential journal. The field's evolution is marked by interdisciplinary integration and branching into various sub-disciplines. CONCLUSIONS Exercise therapy for AS-induced back pain is a growing research area, necessitating further exploration in clinical management and rehabilitation strategies. The relationship between ET and osteoimmunological mechanisms remains a focal point for future research, with a trend towards personalized and interdisciplinary treatment approaches.

lncRNA­MM2P downregulates the production of pro­inflammatory cytokines in acute gouty arthritis.

Acute gouty arthritis (AGA) is characterized by the accumulation of pro­inflammatory cytokines, which are immunological responses to monosodium urate (MSU) crystals. It has been demonstrated that long non­coding RNA (lncRNA)­MM2P is a novel regulator of M2 polarization of macrophages. The aim of the present study was to investigate whether lncRNA­MM2P regulates the MSU­induced inflammatory process. In cell models of RAW 264.7 and THP­1­derived macrophages, decreased expression of lncRNA­MM2P was observed in lipopolysaccharide­ and MSU­treated macrophages, which was accompanied with obvious inflammatory responses. Using small interfering RNA to knockdown lncRNA­MM2P led to the upregulation of MSU­mediated inflammatory responses, both in RAW 264.7 and THP­1­derived macrophages. In conclusion, lncRNA­MM2P could be an important regulator of MSU­induced inflammation, and therefore could be involved in the development of AGA.

Effects of triptolide on the pharmacokinetics of cyclophosphamide in rats: a possible role of cytochrome P3A4 inhibition.

OBJECTIVE: To evaluate the effect of a 10-day course of triptolide (TP) on rat cytochrome (CY) P3A4 activity, and on the pharmacokinetics of cyclophosphamide (CPA). METHODS: In the pharmacokinetics experiment, rats were orally given 0.9% NaCl solution (n=5) and TP [1.2 (mg/kg·d)] for 10 days and a single dose of CPA was administered intravenously (100 mg/kg) to rats on day 11. Blood samples were collected up to 4 h at predetermined time intervals, the plasma concentration of CPA was determined by high performance liquid chromatography (HPLC) and pharmacokinetic parameters were determined. In the in vitro CYP3A4 activity inhibition research, rat blank liver microsomes were divided into 3 groups: a control group, a TS (5 µL, 200 µmol/L) with TP (5 µL, 12.5 µmol/L) group, a TS with ketoconazole (5 µL, 1 µmol/L) group. Concentration of 6ß-hydroxylated testosterone (6ß-OHT) in liver microsomes was measured by HPLC and the activity of CYP 3A4 was calculated through the following formula: Einhibitor/Econtrol × 100%=Cinhibitor/Ccontrol × 100%. RESULTS: Compared with the control group, the area under the plasma concentration-time curve (AUC0-∞) of CPA was significantly increased by 229.05% pretreated with TP (P<0.01). Peak plasma concentrations (Cmax) of CPA was significantly increased and plasma half-life was correspondingly extended. The CYP3A4 activity was significantly inhibited by ketoconazole 93.5%±0.2% and TP 84.6%±0.3% compared with the control group (P<0.01 and P<0.05, respectively). CONCLUSION: Our results strongly suggested that long-term oral intake of TP can distinctly inhibit the CYP3A4 activity and this inhibition evidently decrease the formation of toxic metabolites of CPA.