Propofol postconditioning protects the blood brain barrier by decreasing matrix metalloproteinase9 and aquaporin4 expression and improves the neurobehavioral outcome in a rat model of focal cerebral ischemiareperfusion injury
Propofol, an intravenous anesthetic, inhibits neuronal apoptosis induced by ischemic stroke, protects the brain from ischemia/reperfusion injury and improves neuronal function. However, whether propofol is able to protect the blood brain barrier (BBB) and the underlying mechanisms have remained to be elucidated. In the present study, a rat model of cerebral ischemia/reperfusion was established, using a thread embolism to achieve middle cerebral artery occlusion. Rats were treated with propofol (propofol postconditioning) or physiological saline (control) administered by intravenous injection 30 min following reperfusion. Twenty-four hours following reperfusion, neurobehavioral manifestations were assessed. The levels of cephaloedema, damage to the BBB and expression levels of matrix metalloproteinase-9 (MMP9), aquaporin-4 (AQP4) and phosphorylated c-Jun N-terminal kinase (pJNK) were determined in order to evaluate the effects of propofol on the BBB. In comparison to the cerebral ischemia/reperfusion group, the levels of brain water content and Evans blue content, as well as the expression levels of MMP9, AQP4 and pJNK were significantly reduced in the propofol postconditioning group. These results indicated that propofol postconditioning improved the neurobehavioral manifestations and attenuated the BBB damage and cephaloedema induced following cerebral ischemia/reperfusion. This effect may be due to the inhibition of MMP9 and AQP4 expression, and the concurrent decrease in JNK phosphorylation.
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Document Type: Research Article
Affiliations: Department of Anesthesiology, Sun YatSen Memorial Hospital of Sun YatSen University, Guangzhou, Guangdong 510120, P.R. China
Publication date: August 1, 2015
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