Journal Article Epublish
PubMed: 40104643 DOI: 10.1016/j.mtbio.2025.101589
sLithospermic acid etched ZIF-8 nanoparticles delays osteoarthritis progression by inhibiting inflammatory signaling pathways and rescuing mitochondrial damage.
Mater Today Bio 31:101589
Authors: Yu Zhang, Qiqi Lou, Hao Lian, Ran Yang, Ruolin Cui, Leyang Wang, Bitao Ma, Lingli Hou, Lilun Jin, Weiran Teng
Affiliations
- Department of Traditional Chinese Medicine, School of Medicine, Xinhua Hospital, Afffliated to Shanghai Jiao Tong University, Shanghai, 200092, China.
- Shanghai Institute of Precision Medicine, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China.
Abstract
Osteoarthritis (OA) is the most common chronic inflammatory joint disease. Improving the joint inflammatory microenvironment is expected to promote early intervention and delay the progression of OA. However, effective strategies for inhibiting OA-related joint inflammation are still lacking. Lithospermic acid (LA), a polycyclic phenol carboxylic acid extracted from salvia miltiorrhiza, has strong anti-inflammatory and antioxidant effects. However, its role in the treatment of OA and the underlying mechanisms are unclear. To improve the bioavailability of LA, an LA synergistic protects etched zeolitic imidazolate framework (ZIF)-8 nanoparticles (LA@ZIF-8) was designed and developed for targeted delivery to modulate the inflammatory microenvironment in OA. This study confirmed that LA@ZIF-8 inhibits the pro-inflammatory phenotype of RAW264.7 macrophages through the NF-ĸB signaling pathway, effectively alleviates mitochondrial dysfunction, and delays articular cartilage degeneration caused by the joint inflammatory microenvironment mediated by synoval macrophages. In summary, LA@ZIF-8 delays the progression of OA by inhibiting synovial macrophage-mediated inflammatory responses, highlighting its clinical application potential.
MeSH
Nanoparticles, Macrophages, Osteoarthritis