Moxibustion's Impact on Ferroptosis Regulation: A Key to Relieving Inflammatory Injury in Rheumatoid Arthritis.

Abstract

To study the mechanism through which moxibustion alleviates inflammatory injury of synovial tissue in rheumatoid arthritis (RA) rats model by determining moxibustion's effect on ferroptosis regulation by the tumor suppressor protein p53 and solute carrier family 7 member 11 (SLC7A11). Rats were developed as RA models by the administration of Freund's complete adjuvant. In the corresponding groups, moxibustion treatment was carried out using cigarette-like moxa strips that were suspended near "Shenshu" (BL23) and "Zusanli" (ST36) once daily for 15 days, and the p53 agonist NSC59984 was administered intraperitoneally. After 15 days of treatment, histomorphological changes were noted by transmission electron microscopy; p53, glutathione peroxidase 4 (GPX4), and SLC7A11 expression were detected by Western blot; serum levels of reactive oxygen species (ROS), glutathione (GSH), and Fe²⁺ were estimated with the colorimetric and fluorescent probe methods; and serum levels of tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) were quantified by enzyme linked immunosorbent assay. Compared with the model group and agonist group, the mitochondrial damage in the moxibustion and moxibustion + agonist groups were showed varying degrees of reduction. The levels of p53, ROS, Fe²⁺, TNF-α, and IL-1β in the model group were significantly higher than those in the normal group, the agonist group was significantly higher than the model group, and the moxibustion and moxibustion + agonists groups were lower than the model and agonist groups. The levels of SLC7A11, GPX4, and GSH were the opposite. Moxibustion can improve RA synovial inflammatory injury by regulating ferroptosis through inhibition of p53 protein expression.