Table 2.

Attenuation of endothelial pro-inflammatory activation.

Monoterpene	Experimental Model	Efficacy	Target/Pathway	Refs.
Eucalyptol	HUVECs treated with LPS	Attenuates adhesion molecules and pro-inflammatory cytokines	Regulates PPAR-γ dependent modulation of IκBα/NF- κB signaling	[52]
Citral	HUVECs treated with LPS	Suppresses the adhesion of neutrophils to HUVECs, and decreases adhesion molecules and pro-inflammatory cytokines	Regulates PPAR-γ dependent modulation of IκBα/NF- κB signaling	[53]
Citronellol	Bovine arterial endothelial cells treated with LPS	Suppresses LPS-induced COX-2 expression and attenuates vascular endothelial inflammation	Activates PPARγ signaling	[54]
Genipin	HUVECs treated with TNF-α	Attenuates the adhesion of U937 monocytic cells to HUVECs and ameliorates adhesion molecules	Induces the expression of PPAR-γ	[55]
Cornuside	HUVECs treated with TNF-α	Attenuates pro-inflammatory mediator and adhesion molecules	Suppresses NF-κB signaling	[63]
	HUVECs treated with LPS or HMGB1	Inhibits endothelial permeability, decreases pro-inflammatory mediators, and reduces adhesion events	Modulates SIRT1/HMGB1-mediated NF-κB, ERK and p38 MAPK signaling	[57]
Paeoniflorin	HUVECs treated with LPS	Suppresses the expression of adhesion molecules and pro-inflammatory cytokines	Decreases the activation of IκBα/NF- κB, p38 MAPK and JNK pathway	[61]
	HUVECs treated with ox-LDL	Attenuates adhesion molecule expression	Enhances autophagy via upregulation of SIRT1	[64]
	HUVECs treated with LPC	Suppresses LPC-induced inflammatory factor production	Inhibits the HMGB1-RAGE/TLR-2/TLR-4-NF-κB pathway	[58]
	HUVECs treated with LPS	Suppresses pro-inflammatory cytokines and chemokine	Inhibits ER stress-dependent IRE1α /NF-κB signaling	[65]
Catalpol	Human aortic endothelial cells treated with homocysteine	Inhibits the expression of adhesion molecules and chemokine	Suppresses ER stress and NF-κB signaling	[66]
Geniposide	HUVECs treated with LPS	Inhibits LPS-induced expression of IL-6 and IL-8, and suppresses U937 monocyte adhesion to HUVECs	Attenuates IκBα/NF-κB, p38 MAPK and ERK signaling	[62]
	HUVECs treated with a high level of glucose	Suppresses the adhesion of monocytes to HUVECs and reduces adhesion molecules	Attenuates ROS/NF-κB signaling	[60]
	HUVECs treated with ox-LDL	Decreases the production of pro-inflammatory cytokines	Enhances the miR-21/PTEN pathway	[67]
	ApoE−/− mice fed with HFD and HUVECs treated with H2O2	Suppresses atherosclerosis and inhibits endothelial inflammation	Modulates AMPK/mTOR/Nrf2 signaling pathway	[68]
Bornyl acetate	HUVECs treated with ox-LDL	Suppresses the attachment of THP-1 monocytes to HUVECs, and ameliorates adhesion molecules and pro-inflammatory cytokines	Mitigates the activation of the IκBα/NF-κB signaling pathway	[69]
Carvacrol	C57BLKS/J type 2 diabetic db/db mice and HUVECs treated with a high level of glucose	Alleviates the histological abnormalities of the abdominal aorta and reduces vascular inflammation	Reduces the activation of the TLR4/NF-κB signaling	[70]
Hinokitiol	SEVC4-10 endothelial cells treated with culture medium of LPS-stimulated RAW 264.7 cell	Inhibits pro-inflammatory cytokine-induced adhesion molecules	Not shown	[71]
Thymoquinone	HUVECs treated with LPS	Suppresses pro-inflammatory cytokines and chemokine	Modulates TET2/NLRP3 inflammasome axis	[72]
Amarogentin	C57BL/6J diabetic mice, and EAhy926 cells or HUVECs treated with TNF-α	Exerts anti-atherosclerotic effects and inhibits endothelial inflammation and the adherence of THP-1 monocytes onto HUVECs	Regulates AMPK/NF-κB pathway	[26]
Oleuropein	HUVECs treated with LPS, TNF-α or PMA	Suppresses the adhesion of monocytes to HUVECs and reduces the adhesion molecule VCAM-1	Inhibits the binding of NF-κB, AP-1, and possibly GATA to the promoter of VCAM-1	[73]
Oleacein	HUVECs treated with LPS or TNF-α	Suppresses the adhesion of monocytes to HUVECs and reduces adhesion molecules and pro-inflammatory chemokine	Inhibits NF-κB-mediated CCL2 expression	[74]
Plumericin	HUVECs treated with TNF-α	Attenuates adhesion molecule expression	Regulates IKK/IκB/NF-κB pathway	[75]
Picroside II	HUVECs treated with homocysteine	Reduces the production of inflammatory mediators	Modulates the SIRT1/LOX-1/NF-κB signaling pathway	[76]
Monotropein	HUVECs treated with H2O2	Alleviates the inflammatory response of HUVECs	Attenuates NF-κB/AP-1 signaling	[77]
Albiflorin	HUVECs treated with ox-LDL	Alleviates the production of pro-inflammatory cytokines	Blocks IRAK1/TAK1 pathway	[78]