Table 2.

Available data on tormentic acid activities in NAFLD-related pathologies.

Parameter	Model	Results	Ref.
Steatosis, Lipidemia	In vivo: HFD-fed rats	Inhibition of hyperlipidemia via the activation of the antioxidative mechanisms	[61]
	In vivo: HFD-fed mice	Reduction in body and adipose tissue weights Decreased expression of enzymes involved in fatty acid synthesis	[62]
	In vivo: HFD-fed mice	Reduced visceral fat mass and hepatic triacylglycerol contents Downregulation of SREBP-1c and apo C-III, and upregulation of PPAR-α	[63]
Glucose Homeostasis	In vitro: enzymatic assay	Inhibition of alpha-glucosidase activity	[64]
	In vitro: enzymatic assay	Inhibition of protein tyrosine PTP1B activity	[66]
	In vivo: HFD-fed mice	Decreased levels of blood glucose, insulin, leptin, and HOMA-IR index, and attenuated insulin resistance	[62]
Oxidative Stress	In vitro: rat vascular smooth muscle cells (RVSMCs)	Decreased ROS generation and downregulated the expression of iNOS and NADPH oxidase Prevented phosphorylation of NF-κB subunit p65 and degradation of the NF-κB inhibitor α (IκBα)	[67]
Inflammation	In vitro: rat vascular smooth muscle cells (RVSMCs)	Decreased levels of TNF-α, IL-6, and IL-1β Prevented phosphorylation of NF-κB subunit p65 and degradation of the NF-κB inhibitor α (IκBα)	[67]
	In vivo: acetaminophen-induced liver damage in mice	Inhibition of iNOS and COX-retention of enzymes (essential for the antioxidative properties of the liver): SOD, GPx, CAT Inhibition of NF-κB activation and inhibition of the activation of MAPKs	[68]
	In vitro: LPS-stimulated human gingival fibroblasts (HGFs)	Decreased expression of IL-6 and IL-8 Inhibited LPS-induced TLR4 expression; NF-κB activation; IκBα degradation; and phosphorylation of ERK, JNK, and P38	[69]
	In vitro: LPS-induced inflammation in BV2 microglial cells	Inhibition of TNF-α and IL-1β Activation of LXRα and inhibition of NF-κB activation	[70]
	In vivo: acetaminophen-induced liver damage in mice	Reduction in TNF-α, IL-1β, and IL-6 Inhibition of NF-κB activation and inhibition of the activation of MAPKs	[68]
Fibrosis	In vitro: activated hepatic stellate cells	Decreased the expression of collagen type I and III Prevented excessive deposition of ECM	[71]