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和厚朴酚静脉注射对脑缺血再灌注损伤有保护作用,本研究采用大鼠脑缺血再灌注损伤和自发性高血压易卒中(SHRsp)模型观察口服和厚朴酚微乳对大鼠脑卒中的保护作用。用血管收缩实验、原代大鼠主动脉内皮细胞和原代大鼠脑微血管内皮细胞损伤模型进一步探讨其作用机制。研究结果显示:口服和厚朴酚微乳可明显减小I-R大鼠的脑梗死体积和神经行为学评分,并降低脑组织水含量。该制剂也明显减小SHRsp卒中大鼠的神经行为学评分,显著增加存活率。和厚朴酚明显抑制KCl和苯肾上腺素诱导的大鼠主动脉收缩反应,增加大鼠主动脉内皮细胞NO的释放;NO合成酶抑制剂L-NAME可减弱和厚朴酚对血管收缩的抑制作用。和厚朴酚可增加大鼠主动脉内皮细胞p-eNOS水平和NO的释放。在缺糖缺氧/复糖复氧(OGD)损伤的大鼠脑微血管内皮细胞,和厚朴酚明显增加细胞存活率,增加eNOS和p-eNOS的水平。这些结果提示:和厚朴酚微乳口服对大鼠脑缺血再灌注(I-R)损伤和SHRsp脑卒中具有明显保护作用,这些作用与其内皮细胞保护作用和促进eNOS表达与活化有关。
And honokiol intravenous injection on cerebral ischemia-reperfusion injury in the protection of cerebral ischemia-reperfusion injury in rats and spontaneous hypertensive stroke (SHRsp) model observed oral micro-emulsion of honokiol in rats Stroke protection. Vasoconstriction experiment, primary rat aortic endothelial cells and primary rat brain microvascular endothelial cell injury model to further explore its mechanism of action. The results showed that: oral honokiol microemulsion can significantly reduce I-R rat cerebral infarction volume and neurological behavior score, and reduce water content in brain tissue. The formulation also significantly reduced neurobehavioral scores in SHRsp stroke-treated rats, significantly increasing survival. Honokiol significantly inhibited the contraction of rat aorta induced by KCl and phenylephrine, and increased the NO release in aortic endothelial cells of rats. The NO synthase inhibitor L-NAME attenuated the inhibitory effect of honokiol on vasoconstriction effect. Honokiol can increase the level of p-eNOS and the release of NO in rat aortic endothelial cells. In the rat brain microvascular endothelial cells damaged by hypoxia / hypoxia / reoxygenation (OGD), honokiol significantly increased the cell viability and increased the levels of eNOS and p-eNOS. These results suggest that oral administration of honokiol microemulsion has obvious protective effect on I-R injury and SHRsp stroke, which may be related to the protective effect of endothelial cells and the eNOS expression and activation.