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Previous studies have shown that H 2 S donors or related release systems, such as S-propargyl-cysteine (SPRC), can suppress the expression of M1-related inflammatory factors and promote the formation of M2-like phenotypes, suggesting that the Cys-GSH/H 2 S axis may jointly restrain pro-inflammatory programs by lowering the oxidative stress threshold and modulating signal transduction (79)

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