Table I.

Potential role of Notch signaling in stroke via inflammatory mediators.

Mediator	Source	Potential role in stroke	References
Histamine and serotonin	Mast cells, platelets	Enhancing vascular leakage, regulating cell proliferation and differentiation	74–76
Bradykinin	Plasma substrate	Enhancing vascular leakage and pain	77
C3a	Plasma protein via liver	Enhancing vascular leakage and the formation of opsonic fragment (C3b)	78
C5a	Macrophages	Enhancing vascular leakage, chemotaxis and leukocyte adhesion and activation	79
Prostaglandins	Mast cells from membrane phospholipids	Potentiating other mediators, vasodilation, pain and fever	80,81
Leukotriene B4	Leukocytes	Leukocyte adhesion and activation	82
Oxygen metabolites	Leukocytes	Endothelial damage and tissue damage	22,83–85
IL-1 and TNF-α	Macrophages, other	Acute phase reactions, enhancing vascular leakage and endothelial and tissue damage	18,65,68, 86–89
Chemokines	Leukocytes, others	Leukocyte activation, enhancing vascular leakage and endothelial and tissue damage	90–92
Nitric oxide	Macrophages, endothelium	Vasodilation and cytotoxicity	71

C, complement component; IL-1, interleukin-1; TNF-α, tumor necrosis factor α.