Table 1.

Pharmacological Roles of Ginsengs and Ginsenosides in NAFLD

Disease	Ginseng	Activators/inhibitors	Models	Ref.
NAFLD	KRG	●KRG reduced serum triglyceride level and increased serum HDL level in OLETF rats ●KRG increased NK cell activity in OLETF rats ●KRG ameliorated NAFLD condition in OLETF rats	OLETF rats	[23]
		●KRG improved AST and ALT levels in NAFLD patients ●KRG increased the amounts of Lactobacillus related with improved ALT levels in NAFLD patients	NAFLD patients	[25]
	PNS	●PNS attenuated hepatic steatosis in HFD-treated NAFLD mice ●PNS showed anti-lipogenic and anti-fibrotic activity in HFD-induced NAFLD mice ●PNS reduced gut-to-liver translocation of microbiota fatty acid production in HFD-induced NAFLD mice ●PNS inhibited TLR4 pathways in HFD-induced NAFLD mice	HFD-induced NAFLD mice	[26]
	BG	●BG significantly alleviated NAFLD in HFHF diet-fed mice ●BG reduced lipid accumulation, expression of lipogenic genes, and production of hepatic steatosis molecules in FFA-treated hepatocytes and HFHF diet-fed NAFLD mice	FFA-treated HepG2 HFHF diet-induced NAFLD mice	[27]
	Sap-Rh1/Rg2	●Sap-Rh1/Rg2 improved hepatic steatosis and steatofibrosis in FFD-induced NAFLD mice ●Sap-Rh1/Rg2 suppressed hepatic inflammation by inhibiting NLRP3 inflammasome in FFD-induced NAFLD mice	FFD-induced NAFLD mice	[28]
	KRG-Rd/Rg3	●CRG-Rd/Rg3 prevented hepatic steatosis in FFD-induced NAFLD mice ●CRG-Rd/Rg3 suppressed hepatic lipid accumulation and inflammation in FFD-induced NAFLD mice ●CRG-Rd/Rg3 induced mTORC1-mediated M2 polarization of macrophages	LPS-treated RAW264.7 FFD-induced NAFLD mice	[29]
	Rg1	●Rg1 reduced fat accumulation in hepatocytes ●Rg1 downregulated the apoptosis of steatotic hepatocytes ●Rg1 suppressed SGPL1 expression in steatotic hepatocytes	MCE-treated HHL-5	[30]
		●Rg1 improved liver function in NAFLD rats ●Rg1 prevented fat accumulation and liver damage in NAFLD rats ●Rg1 changed the transcriptome in NAFLD ●Atf3 and Acox2 are key genes for Rg1-mediated efficacy on NAFLD	HFD-induced NAFLD rats	[31]
		●Rg1 ameliorated NAFLD by protecting the livers from hepatic damages, steatosis, and inflammation in D-galactose-induced NAFLD mice ●Rg1 suppressed FOXO1 activation, resulting in the reduction of lipid peroxidation in the livers of D-galactose-induced NAFLD mice	D-galactose-induced NAFLD mice	[32]
		●Rg1 mitigated NAFLD by inhibiting lipid peroxidation and endoplasmic reticulum stress in HFD-induced NAFLD mice ●Rg1 inhibited the activation of the NLRP3 inflammasome, and downregulated the production of the pro-inflammatory cytokines IL-1β and IL-18 in HFD-induced NAFLD mice	HFD-induced NAFLD mice	[33]
	CK	●CK reduced lipid droplet formation in FFA-treated hepatocytes ●CK increased the expression of anti-steatotic genes, such as PPARα and ACOX1, in FFA-treated hepatocytes	FFA-treated HuH7	[36]
		●CK alleviated liver function impairment by mitigating hepatic injury and fibrosis in HFD-induced NAFLD rats ●CK suppressed HSC-T6 cell activation ●CK reduced the expression of PC-I, PC-III, and TIMP-1 in HSC-T6 cells	HSC-T6 HFD-induced NAFLD rats	[37]
	Rh1	●Rh1 alleviated liver function impairment by mitigating hepatic injury and fibrosis in HFD-induced NAFLD rats ●Rh1 suppressed HSC-T6 cell activation ●Rh1 reduced the expression of PC-I, PC-III, and TIMP-1 in HSC-T6 cells	HSC-T6 HFD-induced NAFLD rats	[37]
	Rb2	●Rb2 alleviated hepatic steatosis in db/db mice ●Rb2 restored impaired hepatic autophagy in db/db mice ●Rb2 induced autophagic flux in hepatocytes	HepG2 db/db obese mice	[39]
	Mc1	●Mc1 suppressed palmitate-induced ER stress and apoptosis in hepatocytes ●Mc1 reduced ER stress and hepatic damage in HFD-induced NAFLD mice ●Mc1 ameliorated hepatic steatosis in HFD-induced NAFLD mice	Palmitate-treated HepG2 HFD-induced NAFLD mice	[41]