Melittin acupoint injection in attenuating bone erosion in collagen-induced arthritis mice via inhibition of the RANKL/NF-κB signaling pathway.

Researchers investigated whether melittin acupoint injection (MAI), a traditional Chinese medicine treatment that combines bee venom component with acupuncture points, could help reduce bone damage in rheumatoid arthritis (RA). The study used mice with collagen-induced arthritis, a laboratory model that mimics human RA. The animals received MAI treatments every other day for 28 days at specific acupuncture points. The results showed promising effects. Mice treated with MAI had reduced joint swelling, decreased paw thickness, and lower arthritis severity scores compared to untreated mice. Most importantly, the treatment significantly reduced bone erosion, which is the most serious complication of RA that leads to joint deformities and disability. Imaging studies and microscopic examination revealed that MAI reduced the formation of osteoclasts, the cells responsible for breaking down bone tissue. The treatment also balanced the immune system by decreasing inflammatory molecules like IL-6 and TNF-α while increasing anti-inflammatory molecules like IL-4 and IL-10. Safety testing showed no harmful effects on the liver or kidneys. The researchers discovered that MAI works by blocking a specific cellular pathway called RANKL/NF-κB, which controls osteoclast formation and bone destruction. While these findings are from animal studies and need confirmation in human trials, they suggest that melittin acupoint injection may offer a potential treatment option for preventing bone damage in rheumatoid arthritis. Patients interested in acupuncture-based treatments should consult with a licensed acupuncturist or qualified healthcare provider experienced in treating autoimmune conditions.

This study evaluated melittin acupoint injection (MAI) effects on bone erosion in collagen-induced arthritis (CIA) mice. Treatment was administered every other day for 28 days. MAI significantly improved clinical parameters including arthritis index scores, swollen joint counts, and hind paw thickness (P<0.05 or P<0.01). Micro-CT and histopathological analysis demonstrated marked reduction in bone erosion and osteoclast formation (P<0.01), with TRAP staining confirming decreased osteoclastogenesis. MAI modulated cytokine profiles, reducing pro-inflammatory IL-6 and TNF-α while increasing anti-inflammatory IL-4 and IL-10 (majority P<0.05 or P<0.01). Transcriptome sequencing revealed MAI inhibits the RANKL/NF-κB signaling pathway, a key mechanism in osteoclast differentiation. No hepatic or renal toxicity was observed (P>0.05). Clinical implications suggest MAI may provide a therapeutic approach for preventing bone destruction in RA by simultaneously addressing inflammation and pathological bone resorption through osteoclast regulation.