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首页> 外文期刊>Molecular medicine reports >Propofol post-conditioning protects the blood brain barrier by decreasing matrix metalloproteinase-9 and aquaporin-4 expression and improves the neurobehavioral outcome in a rat model of focal cerebral ischemia-reperfusion injury
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Propofol post-conditioning protects the blood brain barrier by decreasing matrix metalloproteinase-9 and aquaporin-4 expression and improves the neurobehavioral outcome in a rat model of focal cerebral ischemia-reperfusion injury

机译：异丙酚后处理可通过减少基质金属蛋白酶9和水通道蛋白4的表达来保护血脑屏障，并改善局灶性脑缺血再灌注损伤大鼠模型的神经行为结果

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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 post-conditioning) 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 (MMP-9), aquaporin-4 (AQP-4) 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 MMP-9, AQP-4 and pJNK were significantly reduced in the propofol post-conditioning group. These results indicated that propofol post-conditioning 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 MMP-9 and AQP-4 expression, and the concurrent decrease in JNK phosphorylation.
机译：静脉麻醉药异丙酚可抑制缺血性中风引起的神经元凋亡，保护大脑免受缺血/再灌注损伤并改善神经元功能。但是，异丙酚是否能够保护血脑屏障（BBB）及其潜在机制尚待阐明。在本研究中，使用线栓塞术实现脑中动脉闭塞，建立了大鼠脑缺血/再灌注模型。在再灌注后30分钟，通过静脉内注射给予异丙酚（异丙酚后处理）或生理盐水（对照）治疗大鼠。再灌注后二十四小时，评估神经行为表现。测定头水肿水平，对BBB的损伤以及基质金属蛋白酶9（MMP-9），水通道蛋白4（AQP-4）和磷酸化的c-Jun N端激酶（pJNK）的表达水平，以评估其水平。异丙酚对血脑屏障的影响。与脑缺血/再灌注组相比，丙泊酚后处理组的脑含水量和伊文思蓝含量以及MMP-9，AQP-4和pJNK的表达水平显着降低。这些结果表明丙泊酚后处理改善了脑缺血/再灌注后诱导的神经行为表现，并减轻了BBB损伤和头水肿。这种作用可能是由于抑制了MMP-9和AQP-4的表达，以及同时减少了JNK磷酸化。

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