Table 1.

Summary of the roles of endoplasmic reticulum stress and NLRP3 inflammasome in liver disorders.

The Type of Pathological Processes	The Role of ER Stress and the NLRP3 Inflammasome	Experimental Model	Reference
Nonalcoholic hepatitis	ER stress promoted the NLRP3 inflammasome and subsequent pyroptosis and apoptosis to promote nonalcoholic hepatitis	Mouse/mouse primary hepatocyte model of nonalcoholic hepatitis	[46]
Nonalcoholic fatty liver disease (NAFLD)	BI-1 improved NAFLD through inhibition of ER stress-induced and IRE1a-dependent NLRP3 inflammasome activation	Mouse/mouse hepatocyte model of NAFLD	[50]
NAFLD	Rg1 improved NAFLD through the inhibition of ER stress and NLRP3 inflammasome activation	Mouse model of NAFLD	[54]
NAFLD	4-AAQB ameliorated NAFLD through the inhibition of ERS/NLRP3 inflammasome by activating the SIRT1-Nrf2 pathway	Male C57BL/6J mouse model of NAFLD	[56]
Hepatic ischemia–reperfusion(HIRI)	ORY ameliorated HIRI through the inhibition of the NLRP3 inflammasome and ER stress	C57BL/6 mouse model of HIRI	[75]
Hepatotoxicity	Allicin improved AA-induced hepatotoxicity through ER stress inhibition of NLRP3 inflammasome via the MAPK and NF-κB signaling pathways	Sprague Dawley rats/Kupffer cell model of hepatotoxicity	[86]
Hepatotoxicity	BA improved PA-induced cytotoxicity of AML-12 cells through the inhibition of ER stress via the TXNIP/NLRP3 pathway, through the AMPK pathway	AML-12 cell model of hepatotoxicity	[95]
Liver injury	FXR improved liver injury through inhibition of ER stress-induced NLRP3 inflammasome via the PERK–CHOP signaling pathway	C57BL/6J mouse/AML-12 cell model of liver injury	[107]