Table 1.
The effects of GB on leukocyte function.
| Leukocyte subset | Target modulated by GB | Influence of GB on leukocyte subsets in atherosclerosis |
|---|---|---|
| Monocytes | VCAM-1, VE-cadherin, Cx43 | GB suppressed monocyte adhesion in TNF-α-stimulated HUVECs under varied degrees of laminar shear stress39 |
| JAM-A, Cx43, and VE-cadherin | GB inhibited junction protein expression and decreased monocyte transmigration in ox-LDL-treated HUVECs37 | |
| VCAM-1, ICAM-1 | GB suppressed THP-1 monocyte adhesion to TNF-α-induced HUVECs in a dose-dependent manner142 | |
| Macrophages | LOX-1, NOX4, MMP-1, COX-2 | GB decreased cholesterol deposits and showed atherosclerotic protective property35 |
| iNOS, NO | GB antagonized homocysteine-stimulated iNOS-mediated NO production in macrophages through antioxidation and attenuating NF-κB activation143 | |
| Mast cells | PAF-R | GB pretreatment significantly reduced the increase of mast cell degranulation in the rat isolated omentum stimulated by adenosine analogue144 |
| PAF-R | Pretreatment with GB observably decreased PAF's degranulating actions in omental mast cells while significantly reducing PAF's histamine-releasing impact on peritoneal mast cells145 | |
| Neutrophils | PAF-R | GB completely inhibited PAF-induced neutrophil response and subsequent neutrophil-mediated endothelial injury146 |
| [Ca2+]i, PAF-R | GB stimulated intracellular signaling events in neutrophils through tyrosine phosphorylation of proteins, phosphorylation of P38 map kinase, calcium transience, and phospholipase D activity, thus enhancing neutrophils' defense activities147 | |
| PAF-R, CD18, CDllb, superoxide anion | Neutrophils pretreated with GB reduced plasma-mediated neutrophil stimulation after myocardial infarction in the presence of high plasma PAF levels148 | |
| PAF-R | GB specifically suppressed neutrophil activation by blocking the binding of PAF to its receptor on neutrophil149 | |
| PAF-R | GB inhibited PAF-induced chemotaxis of neutrophils150 |