Anemia of
inflammation (AI) is clinically prevalent and greatly threatens public health. Traditional remedies have raised controversy during clinical practice, calling for
alternative therapies. We have recently found that
hydrogen sulfide (H2S) inhibits inflammatory
hepcidin, the critical mediator of AI. However, due to the chemical property of H2S, there remains an urgent need for a stable H2S donor in AI treatment. Here we reported that S-propargyl-
cysteine (SPRC), a novel water-soluble H2S donor, suppressed hepatic
hepcidin and corrected hypoferremia induced by
lipopolysaccharide. The effects of SPRC were reversed by inhibition of
cystathionine γ-
lyase, one of the major endogenous H2S synthases. Moreover, SPRC reduced serum
hepcidin, improved
transferrin saturation, and maintained erythrocyte membrane integrity in a chronic mouse AI model. Consistently,
splenomegaly was ameliorated and splenic
iron accumulation relieved. Mechanism study indicated that serum
IL-6 content and hepatic
Il-6 mRNA were decreased by SPRC, in parallel with reduced hepatic JAK2/STAT3 activation. On the whole, our data reveal the inhibition of inflammatory
hepcidin by SPRC, and suggest SPRC as a potential remedy against AI.