Table 1.
Summary of mechanisms of action of STS in animal models of human diseases.
| Experimental Model | STS Concentration | Effect of STS | References |
|---|---|---|---|
| BCAO-induced cerebral IRI in mice | 10 mg/kg | - Improved neurological function and survival - Inhibitedcaspase-3 activity - Mitigated apoptosis via JNK blocking |
[65] |
| AVF-induced heart failure in mice | 3 mg/mL | - Protected against cardiac dysfunction - Elevated endogenous production of H2S - Prevented the increase in MMP-2, MMP-9, and TIMP-1 expression levels |
[12] |
| Hyperoxaluria in rats | 0.4 g/kg/b.w.t | - Preserved superoxide dismutase activity | [6] |
| Ethylene glycol-induced nephrolithiasis in rats | 400 mg/Kg b.w.t | - Increased renal protection by modulating the mitochondrial KATP channel - Showed normal serum creatinine and renal tissue architecture |
[66] |
| Angiotensin II-induced heart disease in rats | 1 g/kg/day | - Attenuated hypertensive cardiac disease - Regulated blood pressure - Reduced ANP mRNA levels |
[45] |
| Angiotensin II-induced hypertension, proteinuria, and renal damage in rats | 1 g/kg/day | - Increased GSH levels - Reduced influx of macrophages to near-control levels - Improved creatinine clearance |
[4] |
| L-NNA-induced hypertension in rats | 2 g/kg/day | - Enhanced GFT and ERPF - Protected against glomerulosclerosis - Lowered plasma urea and renal vascular resistance |
[67] |
| Myocardial IRI in rats | 1 mM (Postconditioned) |
- Reduced myocardial infarct size - Lowered expression of caspase-3 and PARP |
[68] |
| Renal mitochondrial IRI in rats | 400 mg/kg | - Maintained mitochondrial function - Increased NADH hydrogenase activity |
[14] |
| Myocardial IRI in rats | 1 mM (Preconditioned) |
- Preserved mitochondrial ATP synthesis - Increased PGC-1α expression - Improved ETC complex enzyme activities |
[69] |
| LAD occlusion model of cardiac IRI in rats | 0.1–1 mM | - Reduced apoptosis associated with mitochondrial dysfunction - Lowered levels of cardiac injury markers LHD and CK |
[70] |
| Cardiac IRI with PAG in rats | 1 mM | - Preserved protective mechanisms in presence of PAG | [71] |
| GalN/LPS-induced liver injury in mice | 2 g/kg | - Increased Nrf2 and Akt-dependent signaling - Inhibited JNK phosphorylation |
[21] |
BCAO, bilateral common carotid artery occlusion; STS, sodium thiosulfate; JNK, c-Jun N-terminal kinase; IRI; ischemia–reperfusion injury; GSH, glutathione; AVF, arteriovenous fistula; MMP, matrix metalloproteinases; TIMP, tissue inhibitors of matrix metalloproteinases; ANP, atrial natriuretic peptide; GFR, glomerular filtration rate; L-NNA, N-u-nitro-L-arginine; ERPF, effective renal plasma flow; ETC, electron transport chain; LAD, left anterior descending artery; LHD, lactate dehydrogenase; CK, creatine kinase; PAG, D, L-propargylglycine; GalN, D-galactosamine; LPS, lipopolysaccharide; Nrf2, nuclear factor erythroid related-factor 2.