|
| Experimental models | Effects | Proposed mechanisms | Refs. |
|
| Hepatotoxicity in vivo (rat) | DATS (40 and 80 mg/kg, orally) protects against valproate-induced hepatotoxicity | Antioxidative, anti-inflammatory, and antiapoptotic properties | [159] |
| Hepatotoxicity in vivo (rat) | DADS (10 ml/kg/day) attenuates acetaminophen-induced acute hepatotoxicity | Possibly via the reduction of oxidative stress-mediated JNK activation and the suppression of inflammatory responses | [160] |
| Hepatotoxicity in vivo (mouse) | AMDS (50 mg/kg/day) protects against acetaminophen-induced hepatotoxicity | Through the strong attenuation of the CD45 expression and HNE formation | [161] |
| Hepatotoxicity in vivo (rat) | DATS (80 mg/kg/day) ameliorates arsenic-induced hepatotoxicity | Abrogation of oxidative stress, inflammation, and apoptosis | [162] |
| Hepatotoxicity in vivo (rat) | DADS (2 ml/kg/day) protects against carbon tetrachloride-induced hepatotoxicity | Through activation of Nrf2 | [163] |
| Hepatotoxicity in vivo (rat) | DAS (200 mg/kg/day) ameliorates ferric nitrilotriacetate-induced hepatotoxicity | Unknown | [164] |
| Hepatotoxicity in vivo (mouse) | DATS (40 mg/kg) protects against isoniazid and rifampin-induced hepatotoxicity | Reduction of oxidative stress and activation of Kupffer cells | [165] |
|
