Effects of Anti-intercellular Adhesion Molecule-1 Antibody on Reperfusion Injury Induced by Late Reperfusion in the Rat Middle Cerebral Artery Occlusion Model

Modulation of the balance between cannabinoid CB1 and CB2 receptor activation during cerebral ischemic/reperfusion injury

“…For example, proinflammatory cytokines (TNF-α and IL-1β) secreted by leukocytes not only activate vascular endothelial cells and amplify inflammatory response but also directly induce neuronal injury (Wood, 2003). These studies highlight the involvement of immune cells and inflammatory cytokines in exacerbating ischemic injury, and numerous studies have shown that protection could be offered by interfering the inflammatory responses following ischemic/reperfusion injury (Kanemoto et al, 2002, Weaver et al, 2002, Sughrue et al, 2004. CB 2 is a G i protein coupled-receptor and its activation triggers a series of signal transduction pathways which eventually leads to either up-or down-regulation of gene transcription.…”

Cannabinoid CB2Receptor Activation Decreases Cerebral Infarction in a Mouse Focal Ischemia/Reperfusion Model

“…Matrix metalloproteases (MMPs), secreted by macrophages, can degrade the constituents of basal lamina and thus contribute to blood-brain barrier disruption and cerebral edema during stroke (Maier et al, 2004). All these studies highlight the involvement of white blood cells in exacerbating ischemic injury, and the protection offered by interfering with the ability of white blood cells to adhere to endothelial cells and undergo diapedesis into the brain (Connolly et al, 1996;Heinel et al, 1994;Kanemoto et al, 2002;Vasthare et al, 1990;Weaver et al, 2002;White et al, 2000). In the current investigation, the closed cranial window technique was used to evaluate the effect of selective CB 2 agonists on endothelial/leukocyte interactions.…”

Acute Treatment with Rosuvastatin Protects Insulin Resistant (C57BL/6J ob/ob) Mice against Transient Cerebral Ischemia

“…A series of intracellular events triggered during and after MCAO, including increased calcium release and ROS production, activate second messenger systems such as extracellular signal-regulated kinase (ERK) and promote the expression of proinflammatory proteins and adhesion molecules on the endothelial cell membrane. We and others have previously shown that ICAM-1 expression is correlated with disruption of the blood-brain barrier (Lenzsér et al , 2007) and enhanced infarct volume in rodents (Wang et al , 1994; Zhang et al , 1995), and that suppression of expression or actions of adhesion proteins lessens the severity of injury after MCAO without affecting CBF during ischemia and reperfusion (Vemuganti et al , 2004; Kanemoto et al , 2002). Increased expression of adhesion molecules such as ICAM-1 on endothelial cells interact with complementary surface receptors on neutrophils and allow these blood-borne cells to bind to the endothelium, cross the blood-brain barrier, enter the parenchyma, and initiate inflammatory responses (Schroeter et al , 1994).…”