![]() An important role has been indicated for adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) and p-selectin in the recruitment of leukocytes in the postischemic cerebral microvasculature. ![]() The onset of cerebral ischemia triggers a cascade of proinflammatory molecular and cellular events. It is suggested that apigenin regulates adhesion molecule expression in reactive astrocytes during ischemia. These results suggest that the expression levels of adhesion molecules during H/R affect disease outcome and can drive SHRSP/IZM to stroke. Apigenin strongly attenuated TNF- □-induced VCAM-1 mRNA and protein expression and suppressed the adhesion of U937 cells and SHRSP/IZM astrocytes. The expression of monocyte chemotactic protein-1 (MCP-1) mRNA induced by H/R in SHRSP/IZM astrocytes was increased compared with that in normal oxygen concentrations. ![]() It was found that the expression of vascular cell adhesion molecule-1 (VCAM-1) by TNF- □ in astrocytes isolated from SHRSP/IZM was increased compared with that in WKY/IZM. We examined the possibility that the expression of adhesion molecules is regulated differently in cultured astrocytes from stroke-prone spontaneously hypertensive rats (SHRSP/IZM) rats than in those from Wistar Kyoto rats (WKY/IZM) by tumor necrosis factor-alpha (TNF- □) or hypoxia and reoxygenation (H/R) and the inhibitory effects of apigenin.
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