Table 2.

Possible molecular targets to develop antifibrotic drugs.

Target	Model	Molecule	Effect	Ref.
ROS	NASH	Vitamin E	Protected the structural components of the cell membrane from peroxidation	[176]
ROS	ALD and NALD	Silibinin	Increased glutathione concentrations, reversed fibrosis, and stimulated regeneration	[74,75]
CYP2E1	ALD	Diallyl sulfide and phenethyl isothiocyanate	Prevented the production of lipid peroxide and the accumulation of important fatty acids and reduced the pathology score	[177,178]
CYP2E1	ALD	Chlormethiazole	Reduced the proteasome proteolytic enzyme activity induced by ethanol feeding	[179]
NO	ALD	Nostrin	Decreased enzymatic activity of endothelial nitric oxide synthase	[180]
NRF2	ALD	Ethyl pyruvate	Increased anti-inflammatory factors	[181,182]
NRF2	NAFLD and NASH	NRF2 activators	Prevented inflammation, triglyceride accumulation, and fibrosis in the liver	[159,163,165,166,167,168,169].
NLPR3	NASH	MCC950	Normalized hepatic caspase 1 and IL-1β expression, plasma IL-1β, MCP-1 and IL-6, lowered ALT/AST, and reduced the severity of liver inflammation	[183]
Caspases	NASH	Emricasan	Ameliorated liver injury and fibrosis	[184]
Caspases	NASH	GS-9450	Reduced ALT levels in NASH patients	[185]
Caspases	NASH	VX-166	Inhibited collagen gene expression and reduced hepatic accumulation of cells expressing the myofibroblast marker α-SMA	[186]

NASH, nonalcoholic steatohepatitis; ALD, alcoholic liver disease; NALD, nonalcoholic liver disease; NAFLD, nonalcoholic fatty liver disease; ALT, alanine aminotransferase; AST, Aspartate aminotransferase.