Vascular Protective Effect and Its Possible Mechanism of Action on Selected Active Phytocompounds: A Review

Table 1

Summary of the type of endothelial cell damaging factors with its effects on respective vascular endothelial cells.

Source	Type of endothelial cell	Effect/mechanism	Ref.
Tumor necrosis factor-alpha (TNF-α)	Human umbilical vein endothelial cells (HUVECs)	(i) Induction of oxidative stress, inflammation, and apoptosis; (ii) Induction of inflammation and monocytes adhesion	[28,29]
Glycated low-density lipoprotein (glyLDL)	Porcine aortic EC (PAEC)	(i) Induction of oxidative stress and apoptosis	[30]
Bradykinin	HUVECs	(i) Induction of endothelial hyperpermeability; (ii) Stimulation of angiogenesis via increased endothelial permeability and remodeling	[31,32]
Histamine	HUVEC; Human dermal microvascular endothelial cells (HDMEC)	(i) Increased endothelial permeability through PLC-NO-cGMP signaling cascade; (ii) Induction of endothelial dysfunction by activating Ca2+-mediated RhoA and adherens junctions’ tension	[33,34]
α-Thrombin	HUVECs	(i) Increased endothelial macromolecular permeability	[35]
IFNγ	HUVEC	(i) Induction of endothelial hyperpermeability via activation of p38 MAP kinase and actin cytoskeleton alteration	[36]
IL-1α	Brain microvascular endothelial cells (BECs)	Activation and induction of angiogenic markers in endothelial cells	[37]
IL-1β	Human glomerular endothelial cell (HRGEC)	Induction of vascular hyperpermeability and upregulation of vascular endothelial-cadherin	[38]
IL-4	Human coronary artery endothelial cells (HCAEC) and human pulmonary artery endothelial cells (HPAEC)	Induction of vascular hyperpermeability through Wnt5A signaling	[39]
Lipopolysaccharide (LPS)	HUVECs; HUVECs and human lung microvascular endothelial cells (HMVEC-L)	(i) Induction of apoptosis, injury, JNK phosphorylation, decreased MCL-1 expression and SOD activity, and increased proinflammatory cytokine production.; (ii) Activation of endothelial cells’ inflammatory responses	[40,41]
Thrombin	Primary human dermal microvascular endothelial cells (HDMECs); Human pulmonary microvascular endothelial cells (HPMVECs)	(i) Induction of microvessel leakage; (ii) Induction of vascular hyperpermeability via dysregulation of vascular endothelial (VE-)cadherin and alteration of small rho GTPases	[42,43]
Angiotensin II (Ang II)	HUVECs	Induced vascular endothelial cells’ injury and oxidative stress	[44]
Glucose	Rat aortic endothelial cells (RAOECs)	Induces cyclin D2 upregulation and miR‐98 downregulation	[45]