论文部分内容阅读
目的研究脑脉泰胶囊对大鼠局灶性脑缺血再灌注损伤血脑屏障和脑水肿的影响。方法大脑中动脉线拴法(MCAO)制作大鼠局灶性脑缺血再灌注模型:雄性SD大鼠随机分为假手术组(sham)、脑缺血再灌注模型组(MCAO)、脑脉泰大、中、小剂量组(MCAO+脑脉泰2.2,1.1,0.6 g.kg-1)和尼莫地平组(MCAO+尼莫地平1×10-2 g.kg-1),每组10只大鼠。大鼠大脑中动脉阻断1.5 h,再灌注24 h。伊文思兰(EB)法测定血脑屏障的损伤程度;用TUNEL法和免疫组化染色法分别检测缺血半暗带凋亡细胞和水通道蛋白(AQP4)的表达;电镜观察脑组织超微结构。结果脑脉泰大、中2个剂量能显著减少大鼠实验性局灶性脑缺血的EB含量、降低脑含水量,脑缺血半暗带的凋亡细胞显著减少,AQP4表达减少,与MCAO模型组比较,有显著性差异(P<0.05)。电镜显示MCAO模型组神经细胞胞质水肿,神经元核不规则,核膜断续,线粒体肿胀、嵴断裂或空泡化,粗面内质网扩张。与MCAO模型组比较,脑脉泰组大鼠神经细胞水肿和线粒体损伤明显减轻。结论脑脉泰对脑缺血/再灌注损伤的保护作用和减轻脑水肿的机制,可能与抑制神经细胞凋亡,降低AQP4蛋白的表达,减少线粒体和血脑屏障的损伤有关。
Objective To study the effect of Naomaitai capsule on the blood-brain barrier and cerebral edema in rats with focal cerebral ischemia-reperfusion injury. Methods The rat model of focal cerebral ischemia and reperfusion was established by middle cerebral artery occlusion (MCAO). Male SD rats were randomly divided into sham group, cerebral ischemia-reperfusion model group (MCAO), and cerebral veins. Tai Da, medium, and small dose groups (MCAO+ Nao Mai Tai 2.2, 1.1, 0.6 g.kg-1) and Nimodipine group (MCAO+ Nimodipine 1×10-2 g.kg-1), 10 in each group Rats. The middle cerebral artery was blocked for 1.5 h and reperfused for 24 h. Evans blue (EB) method was used to measure the degree of blood-brain barrier injury. Apoptotic cells and aquaporin (AQP4) expression in the ischemic penumbra were detected by TUNEL and immunohistochemical staining. Electron microscopy was used to observe ultrastructure of brain tissue. structure. RESULTS: Both Namai Taida and Zhongda doses significantly reduced the EB content and the brain water content in experimental focal cerebral ischemia in rats. The apoptotic cells in the cerebral ischemic penumbra were significantly reduced, and the expression of AQP4 was decreased. Compared with the MCAO model group, there was a significant difference (P<0.05). Electron microscopy revealed that the MCAO model group had neuronal cytoplasmic edema, irregular neuronal nuclei, intermittent nuclear membranes, mitochondrial swelling, sacral breaks or vacuolization, and rough endoplasmic reticulum expansion. Compared with the MCAO model group, neuronal edema and mitochondrial damage were significantly reduced in the rats of Naomaitai group. Conclusion The protective effect of Nao Mai Tai on cerebral ischemia/reperfusion injury and the mechanism of reducing cerebral edema may be related to inhibiting neuronal apoptosis, reducing the expression of AQP4 protein, and reducing the damage of mitochondria and blood-brain barrier.