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目的探讨胡黄连苷Ⅱ对大鼠缺血损伤脑组织中水通道蛋白4(AQP4)表达的影响。方法 Wistar大鼠60只,选取15只为对照组(不结扎双侧颈总动脉),其余45只应用双侧颈总动脉结扎法建立大鼠前脑缺血模型(成模30只,再随机分为模型组和治疗组,均n=15只),治疗组成模2 h后经腹腔注射胡黄连苷Ⅱ10 mg·kg-1干预治疗。测定各组脑组织含水量,酶联免疫吸附法检测脑组织AQP4含量,免疫组化法观察缺血区AQP4阳性细胞表达,透射电镜观察缺血区超微结构。结果治疗组脑组织含水量、AQP4阳性细胞指数、变性细胞指数均较模型组显著降低(P<0.05);治疗组脑组织AQP4含量较模型组显著降低(P<0.01);对照组血管内皮细胞,基底膜清晰完整;神经细胞结构正常,轮廓清晰,染色质均匀;模型组血管内皮细胞质溶坏死、基底膜消失;神经细胞形态欠规整,出现凋亡、坏死现象。治疗组血脑屏障及神经细胞损伤较模型组明显减轻。结论胡黄连苷Ⅱ通过下调AQP4的表达,减轻脑缺血对血脑屏障及神经细胞的损伤。
Objective To investigate the effect of picroside Ⅱ on the expression of aquaporin 4 (AQP4) in ischemic brain tissue of rats. Methods Fifty-six Wistar rats were selected as the control group (without bilateral carotid artery ligation), and the other 45 rats were subjected to bilateral common carotid artery ligation to establish an anterior cerebral ischemia model Divided into model group and treatment group, all n = 15). After 2 h of treatment, the model group and the treatment group were treated by intraperitoneal injection of picrotoxin Ⅱ 10 mg · kg-1. The content of AQP4 in brain tissue was measured by enzyme-linked immunosorbent assay. The expression of AQP4 positive cells was observed by immunohistochemical method. The ultrastructure of ischemic area was observed by transmission electron microscopy. Results The content of AQP4, the index of AQP4-positive cells and the index of degenerative cells in the treatment group were significantly lower than those in the untreated group (P <0.05). The content of AQP4 in the treated group was significantly lower than that in the untreated group (P <0.01) , The basement membrane was clear and complete; the structure of nerve cells was normal, the outline was clear and the chromatin was uniform; the vascular endothelial cells in model group were dissolved and necrotic, the basement membrane disappeared; and the morphology of nerve cells was irregular and apoptotic and necrotic. Blood-brain barrier and nerve cell injury in the treatment group were significantly reduced compared with the model group. Conclusion Picroside II can reduce the damage of blood brain barrier and nerve cells by decreasing the expression of AQP4.