Table 1.

Effects of pharmacologic activation of FXR on drug-induced liver injury.

Compound	Etiopathogenesis of Liver Disease	Type of Study	Outcome	Ref.
GW4064	Acetaminophen-induced toxicity	Mouse	-Reduced serum ALT, AST and TNFα levels -Reduced liver necrosis	[126]
GW4064	Acetaminophen-induced toxicity	In vitro Mouse	-Upregulation of glutathione cycle genes -Reduced serum ALT, AST and LDH levels -Reduced liver necrosis	[130]
GW4064	Amoxicillin/Clavulanic acid-induced toxicity	In vitro	-GW4064 failed to activate FXR in cells treated with clavulanic acid.	[133]
Schaftoside	Acetaminophen-induced toxicity	Mouse	-Upregulation of glutathione cycle genes -Reduced serum, AST and LDH levels -Reduced hepatic oxidative stress and inflammation	[127]
Saffron	Acetaminophen-induced toxicity	Rat	-Reduced serum ALT, AST and LDH levels -Reduced hepatic glycogen depletion, sinusoidal dilation, vacuolization, bile stasis and necrosis	[128]
OCA	Tripterygium-induced toxicity	Mouse	-Reduced serum ALT, AST, ALP and TBA -Reduced histological alterations	[131]
OCA	Valproic acid-induced toxicity	In vitro Mouse	-Upregulation of glutathione cycle genes -Reduced hepatic oxidative stress -Reduced hepatic steatosis -Reduced hepatic oxida-tive stress -Upregulation of glutathione cycle genes -Downregulation of PPARγ gene	[132]

ALP = alkaline phosphatase, ALT = alanine aminotransferase, AST = aspartate transaminase, FXR = farnesoid X receptor, LDH = lactate dehydrogenase, PPARγ = peroxisome proliferator-activated receptor, OCA = Obeticholic acid, TBA = total bilirubin.