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] |