Figure legends
Figure 1. Endogenous hydrogen sulfide can be produced by two
ways: Enzyme catalysis and non Enzyme catalysis. Enzyme catalysis is the
main way and is catalyzed by four enzymes, such as CBS, CSE, MST and
DAO. By Figdraw.
H2S: Hydrogen sulfide; CBS: cystathionine β‑synthase; CSE: cystathionine
γ‑lyase; PLP: pyridoxal-5’-phosphate; 3-MST: 3-mercaptopyruvate
sulfurtransferase; 3-MP: 3-methylpyridine; CAT: Cysteine
aminotransferase; DAO:D-amino acid oxidase.
Figure 2. The H2S oxidation pathway in
mitochondria is mainly catalyzed by sulfuroquinone oxidoreductase.
Finally, hydrogen sulfide is discharged from the body in the form of
Thiosulfate or sulfate through this pathway. By Figdraw.H2S: Hydrogen
sulfide; SQR: sulfuroquinone oxidoreductase; GSH: glutathione; GSSH:
glutathione disulfide; TST: rhodanese; SDO: sulfide dioxygenase; Cyt
c:cytochrome c oxidase; ATP: adenosine triphosphate; ADP:adenosine
diphosphate; NADH: Nicotinamide adenine dinucleotide.
Figure 3.The mechanism of ion exchange leading to calcium
overload during the ischemic and reperfusion stages. By Figdraw. ATP:
adenosine triphosphate; CaBP: calcium binding protein;
Na+: sodium ion; Ca2+: calcium ion;
K+: potassium ion; H+: hydrogen ion.
Figure 4.H2S can reduce the infarct size of
cerebellar tissue and restore neurological function through mechanisms
such as antioxidant, anti-inflammatory, anti-apoptotic, regulating
autophagy, protecting mitochondrial function, and vasodilation and
generation. By Figdraw. ATP: adenosine triphosphate; NF-κB: nuclear
factor-kappa B; TNF-α: tumor necrosis factor-α; COX-2: cytochrome
oxidase subunit 2; ROS: reactive oxygen species; iNOS: Inducible nitric
oxide synthase;γ-GCS: γ-glutamylcysteine synthetase; VEGF: Vascular
endothelial growth factor; mPTP: mitochondrial permeability transition
pore.