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目的:探讨小檗碱对缺血性脑损伤2型糖尿病大鼠脑组织AQP1表达的影响。方法:高脂高糖饲养健康SPF级Sprague-Dawley雄性大鼠8周后,腹腔单次注射链脲佐菌素(streptozotocin,STZ)(30mg/kg),3d后测大鼠血糖浓度大于16.7mmol/L即为糖尿病模型;采用Zea Longa等的改良线栓法制备大鼠局灶性脑栓塞模型。实验分4组进行:(1)假手术组;(2)模型组(糖尿病+脑缺血模型);(3)BBR组(模型+小檗碱);(4)甘露醇对照(模型+甘露醇)组,处理期间继续按原方法喂养。分别于缺血后12、16、20、24h经股静脉穿刺给药,小檗碱剂量为0.05g/kg体重,甘露醇剂量为0.5g/kg体重,给药时间为5min~10min,实验结束采血取材。用神经功能缺损评分(NIHSS)对大鼠一般状态进行评估;用脑组织含水量检测评估脑水肿程度;H·E染色光镜观察脑组织的病理改变和脑水肿程度;免疫组织化学和免疫印迹法检测脑组织中AQP1的表达情况。结果:小檗碱处理组2型糖尿病大鼠一般状况好于模型组,脑水肿减轻;H·E染色显示,小檗碱处理组脑组织的神经元胞体水肿不明显,模型组水肿明显;免疫组织化学和免疫印迹法检测小檗碱处理组脑组织的AQP1表达明显降低。结论:小檗碱可减轻2型糖尿病大鼠脑缺血损伤的病理变化;小檗碱处理组2型糖尿病大鼠脑组织AQP1表达降低。
Objective: To investigate the effect of berberine on the expression of AQP1 in cerebral tissue of type 2 diabetic rats with ischemic brain injury. Methods: Healthy Sprague-Dawley male Sprague-Dawley rats were injected with streptozotocin (STZ) (30mg / kg) intraperitoneally once a day for 8 weeks. After 3 days, the blood glucose level of rats was more than 16.7mmol / L is the diabetic model; using Zea Longa and other improved thread method rat focal cerebral embolism model. The experiment was divided into 4 groups: (1) sham operation group; (2) model group (diabetic + cerebral ischemia model); (3) BBR group (model + berberine); Alcohol) group, continue to feed the original method during treatment. The rats were administered with femoral vein puncture 12, 12, 20, 24 h after ischemia respectively. The dose of berberine was 0.05 g / kg body weight, the dosage of mannitol was 0.5 g / kg body weight, and the administration time was 5 min-10 min. Blood drawn. The neurological deficit score (NIHSS) was used to assess the general state of rats; brain water content was used to assess the extent of brain edema; H · E staining was used to observe the pathological changes of brain tissue and brain edema; immunohistochemistry and immunoblotting Method to detect the expression of AQP1 in brain tissue. Results: The general condition of type 2 diabetic rats treated with berberine was better than that of the model group, and the edema of brain was relieved. The H · E staining showed that the edema of neuronal soma was not obvious in the brain tissue of berberine treated group, Histochemistry and Western blotting showed that the expression of AQP1 in brain tissue of berberine-treated group was significantly decreased. CONCLUSION: Berberine can reduce the pathological changes of cerebral ischemia injury in type 2 diabetic rats, and reduce the expression of AQP1 in type 2 diabetic rats treated with berberine.