Table 1.
Previous studies on the effects of H2S in acute kidney injury.
| Model | Protocol | Treatment | Dose | Effect of H2S | Mechanism | Reference |
|---|---|---|---|---|---|---|
| male C57BL/6 mice ischemia/reperfusion injury | I (30 min)/R (8 days) | NaHS | 500 μg kg–1 BW | –accelerated the recovery of renal function and tubule morphology | –reduced post–I/R superoxide formation, lipid peroxidation, GSSG/GSH level and Nox4 expression –increased catalase and SOD expression |
[37] |
| CSE−/− mice ischemia/reperfusion injury | I (30 min)/R (1 day) | intraperitoneal injection of NaHS 15 min before surgery | 1 mg kg–1 | –decreased mortality and severity of damage | –regulated the amount of ROS associated with hypoxic stress | [38] |
| male Wistar rats ischemia/reperfusion injury | I (50 min)/R (1 day) | intraperitoneal injections of NaHS 10 min before the onset of ischemia and immediately after the onset of reperfusion | 75 μmol kg–1 | –attenuated the severity of the structural changes | –reduced oxidative stress | [39] |
| male C57BL/6 mice Cisp–induced AKI | Single injection of 16 mg kg–1 Cisp | intraperitoneal injections of NaHS for 4 days | 5.6 mg kg–1 day–1 | –prevented mitochondrial dysfunction –increased ATP generation –decreased oxidative injury |
–increased S–sulfhydration of SIRT3 –induced deacetylation of OPA1, ATP synthase β, and superoxide dismutase 2 protein |
[53] |
| male Sprague–Dawley rats Cisp–induced AKI | injection of 6 mg kg–1 Cisp | single dose of NaHS | 100 µmol kg–1 | –attenuated proximal tubular cell apoptosis and mesangial matrix | –exhibited antioxidant properties | [56] |
| male Sprague–Dawley rats Cisp–induced AKI | injection of 25 mg kg–1 Cisp | intraperitoneal injections of NaHS and CYY4137 for 4 days | NaHS 5.6 mg kg–1 GYY4137 100 mg kg–1 |
–attenuated proximal tubule cell death and nephrotoxicity | –suppressed intracellular ROS generation –blocked downstream MAPKs by inhibiting NADPH oxidase activity |
[65] |
| male C57BL/6 mice Cisp–induced AKI | injection of 25 mg kg–1 Cisp | intraperitoneal injections of NaHS and CYY4137 for 4 days | NaHS 5.6 mg kg–1 GYY4137 100 mg kg–1 |
–reduced tubular injury | –suppressed the massive production of inflammatory cytokines –decreased phosphorylation of STAT3 and IKKβ –mitigated phosphorylation and degradation of IκBα |
[66] |
| male Swiss albino mice LPS–induced AKI | injection of 10 mg kg–1 LPS 6 h | intraperitoneal injections of NaHS 30 min before LPS | 14 μmol kg–1 | –damaged glomerular hypercellularity | –exhibited proinflammatory activity | [64] |
| male wild–type C57BL/6 J mice LPS–induced AKI | injection of 5 mg kg–1 LPS 6 h | intraperitoneal injections of NaHS 3 h after LPS | 50 μmol kg−1 | –improved renal function and attenuated kidney histopathological changes | –inhibited inflammation and oxidative stress via the TLR4/NLRP3 signaling pathway | [67] |
| male C57BL/6 mice LPS–induced AKI | injection of 10 mg kg–1 LPS 12 h | intraperitoneal injections of NaHS 30 min before LPS | 0.8 mg kg–1 | –improved edema and granular degeneration of tubular epithelial cells | –promoted autophagy –inhibited apoptosis –induced release of inflammatory factors |
[68] |
Abbreviations: NaHS (sodium hydrosulfide); I/R (ischemic/reperfusion); GSSG (glutathione disulfide); GSH (glutathione); SOD (superoxide dismutase); CSE (cystathionine gamma–lyase); ROS (reactive oxygen species); STAT3 (signal transducer and activator of transcription 3); OPA1 (optic atrophy 1); IKKβ (IkappaB kinase beta); IκBα (IkappaB alpha); LPS (lipopolysaccharide); TLR4 (toll–like receptor 4); NLRP3 (NOD–like receptor family pyrin domain–containing 3).