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. Author manuscript; available in PMC: 2016 Sep 1.
Published in final edited form as: Trends Pharmacol Sci. 2015 Jun 9;36(9):568–578. doi: 10.1016/j.tips.2015.05.007

Figure 4.

Figure 4

Hypothetical mechanisms responsible for anti-inflammatory effects of endogenous or exogenous H2S. H2S may exert its anti-inflammatory effects via modulating a variety of signaling mechanisms including NfKB, Nrf-2, or IL-10/JAK/STAT3-dependent signaling. Thiosulfate may also exert anti-inflammatory effects. The solid arrow lines depict the stimulatory interactions whereas the dotted barbed lines indicate the inhibitory interactions. Met, methionine; Hcy, homocysteine; Cys, cysteine; CAT, cysteine aminotransferase; CBS, cystathionine beta-synthase; CSE, cystathionine gamma-lyase; MST, 3-mercaptopyruvate sulfurtransferase; Nrf2, Nuclear factor (erythroid-derived)-like 2; JAK, janus kinase; STAT, signal transducer and activator of transcription; SQR, sulfide quinone oxidoreductase; SDO, sulfide dioxigenase; SO, sulfite oxidase; TST, thiosulfate sulfurtransferase.