Catechin Mediates Ferroptosis to Exert an Anti-Inflammatory Effect on RAW 264.7 Cells

Catechin possesses a potential anti-inflammatory activity, but its anti-inflammatory mechanism is still unclear. Herein, the analysis of network pharmacology showed that catechin might mediate ferroptosis on macrophages to exhibit a significant anti-inflammatory effect on RAW264.7. The metabolomics further indicated that catechin might influence ferroptosis by activating two pathways of cysteine and methionine metabolism and glutathione metabolism, and inhibiting the pathway of ferroptosis to promote the reduction of 1-methionine-s-oxide and s-glutathionyl-1-cysteine, and the reduction and synthesis of gamma-glutamylcysteine. Furthermore, related proteins (MSRA, CDR, GSR and GCL) in three metabolic pathways and ferroptosis-related proteins (GPX4 and SLC7A11) might be relevant to catechin through molecular docking. Thus, we speculate that catechin plays an anti-inflammatory effect through mediating ferroptosis on RAW264.7, which still needs further focus on the detailed molecular mechanism.

Automated summary

Catechin may exert an anti-inflammatory effect through mediating cellular ferroptosis. It appears to influence ferroptosis by activating cysteine and methionine metabolism and glutathione metabolism, while inhibiting the ferroptosis pathway. Several proteins in these metabolic pathways, as well as GPX4 and SLC7A11, which are related to ferroptosis, may be relevant to catechin through molecular docking.