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. 2020 Mar 13;10(3):445. doi: 10.3390/biom10030445

Table 1.

Summary of exemplary beneficial effects of H2S and CO.

H2S
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Reference CO
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Reference
Beneficial effects of H2S and CO
Anti-inflammatory decreased serum level of TNF-α and IL-1β and expression of mRNA in gastric mucosa [5,15] inhibited production of TNF-α, IL-1β in LPS-stimulated macrophages in vivo and in vitro [44]
reduced mRNA and protein expression of HIF-1α in gastric mucosa [5,15] increased IL-10 expression in macrophages via activation p38MAPK [87]
supressed NF-κB pathway in gastric mucosa [21] decreased ERK1/2 kinase activity in T cells [88]
induced activation of AnxA1 pathway [21] re reduced mRNA and protein expression of HIF-1α in gastric mucosa and supressed NF-κB pathway in gastric mucosa [15]
involved in regulation of Th1, Th2, and Th17 lymphocyte differentiation, decrease of IL-17A content [50]
Anti-oxidative caused Nrf-2 /HMOX-1pathway upregulation [11,18] inhibited the lipid peroxidation [2]
decreased level of MDA and increased production of glutathione (GSH) [7,56] decreased level of MDA and modulated SOD activity [56,89]
Vasodilatation increased gastric microcirculation via sGC on endogenous NO and CO biosynthesis-dependent manner [53,54,56] Increased gastric microcirculation via sGC with contribution of NO biosynthesis pathway and independently on endogenous H2S activity [40,42,43,54,56]
dependent on activation of KATP channels [90] dependent on activation of KATP channels [91]
HCO3- secretion in duodenum increased [64] increased [62,64]
Impact on gut microbiota caused the reconstitution of microbiota biofilm dysbiosis [69,72] found to be involved in CO/HMOX-1 pathway in cross-talk between the microbiota and the mucosal immune compartment [49]
Cross-talk between H2S and CO
Direction Mechanism of action Possible biological effect References
CO→ ↓ H2S CO can bind to CBS and inhibits its activity switch of transsulfuration pathway into the remethylation pathway→ methylation of proteins→ epigenetic changes [76,77]
H2S → ↑CO H2S activates Nrf-2 which and modulates of HMOX-1 expression and CO production modulation of oxidative homeostasis and Nrf-2-dependent molecular pathways [18]