Table 3.
Protective effects of H2S on NAFLD/NASH.
| Experimental models | Effects | Proposed mechanisms | Refs. |
|---|---|---|---|
| NAFLD in vivo (mouse) | NaHS (56 μmol/kg/day) attenuates HFD-induced NAFLD | Activation of liver autophagy via the AMPK-mTOR pathway | [138] |
| NAFLD in vivo (mouse) | NaHS (50 μmol/kg/day) mitigates HFD-induced NAFLD | Improvement of lipid metabolism and antioxidant potential | [49] |
| NAFLD in vivo (mouse) | NaHS (14 μmol/kg) attenuates concanavalin A-induced hepatitis | Inhibition of apoptosis and autophagy partly through activation of the PI3K-AKT1 signaling pathway | [139] |
| NASH in vivo (rat) | NaHS (28 μmol/kg/day) attenuates MCD-induced NASH | Possibly through abating oxidative stress and suppressing inflammation | [22] |
| NAFLD in vivo (mouse) | SPRC (an H2S donor, 40 mg/kg/day) exerts a novel protective effect on MCD-induced NAFLD | Antioxidative effect through the PI3K/Akt/Nrf2/HO-1 signaling pathway | [50] |
AMPK: adenosine monophosphate-activated protein kinase; mTOR: mammalian target of rapamycin; PI3K: phosphatidylinositol 3-kinase; MCD: methionine-choline-deficient; HO-1: heme oxygenase-1.