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.