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目的:研究黄芩苷/栀子苷配伍(7:3)对脑缺血再灌注损伤大鼠神经功能损伤的修复作用及作用机制。方法:采用改良线栓法制作脑缺血再灌注损伤模型,造模后24 h,采用平衡木试验、大鼠抓力测定法进行评价神经功能缺损,ELISA法观察脑组织中Na~+、K+-ATP酶、Ca~(2+)、Mg~(2+)-ATP酶活性大小,尼式(Nissl)染色法检测大鼠冠状脑区皮质神经元的形态和数量,免疫组织化学检测脑组织中水通道蛋白-4((aquaporin-4,AQP-4)、胶质纤维酸性蛋白(glial fibrillary acidic protein,GFAP)的表达。结果:与模型对照组相比,黄芩苷/栀子苷配伍治疗组能降低神经功能损伤,减少进入血管外及细胞间的颗粒、减轻血管内皮细胞水肿,增加Nissl阳性细胞的数量,升高脑组织中Na~+、K+-ATP酶、Ca~(2+)、Mg~(2+)-ATP酶活力,下调AQP-4蛋白、GFAP蛋白表达,其中,黄芩苷、栀子苷配伍(42+18 mg/kg.d)组有显著性差异。结论:黄芩苷/栀子苷配伍能够减轻CIRI脑水肿,对大鼠缺血再灌注脑损伤的神经保护作用可能与增加Na~+、K+-ATP酶、Ca~(2+)、Mg~(2+)-ATP酶活力,下调AQP-4及GFAP蛋白表达有关。
Objective: To investigate the repair effect and mechanism of baicalin / geniposide (7: 3) on neurological injury induced by cerebral ischemia-reperfusion injury in rats. Methods: The model of cerebral ischemia - reperfusion injury was made by modified thread method. After 24 h of modeling, the rats were evaluated by balance beam test and rat ’s gravitation test to evaluate the neurological deficits. The levels of Na +, K + ATPase, Ca ~ (2 +) and Mg ~ (2 +) - ATPase activities were detected by enzyme-linked immunosorbent assay (ELISA). Nissl staining was used to detect the morphology and number of cortical neurons in rat coronal brain regions. Immunohistochemistry The expressions of aquaporin-4 (AQP-4) and glial fibrillary acidic protein (GFAP) were detected by ELISA.Results: Compared with the model control group, the combination of baicalin and geniposide treatment group Can reduce neurological damage, reduce entry of extravascular and intracellular particles, reduce vascular endothelial cell edema, increase the number of Nissl positive cells, increased brain Na +, K + -ATPase, Ca ~ (2+), Mg 2+ -ATPase activity, down-regulating the expression of AQP-4 protein and GFAP protein, among which baicalin and geniposide had significant difference (42 + 18 mg / kg.d) / Geniposide can reduce CIRI cerebral edema, cerebral ischemia-reperfusion injury in rats with neuroprotective effects may be increased Na ~ +, K + -ATPase, Ca ~ (2+ ), Mg ~ (2 +) - ATPase activity and down-regulating the protein expression of AQP-4 and GFAP.