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作 者:汝亚琴[1] 金智生[2] 张花治[2] 李桂珍[2]
机构地区:[1]甘肃省康复中心医院眼科,甘肃兰州730000 [2]甘肃中医药大学中医临床学院,甘肃兰州730000
出 处:《兰州大学学报(医学版)》2015年第4期15-19,共5页Journal of Lanzhou University(Medical Sciences)
基 金:国家自然科学基金地区科学基金项目(81160427)
摘 要:目的探讨红芪多糖(HPS)对db/db小鼠视网膜血管内皮生长因子(VEGF)表达的影响。方法 50只db/db小鼠随机分为糖尿病模型组,依那普利组,HPS200m酽略组、100mg/k【g组、50mg/kg组,每组10只。同品系非糖尿病db/m小鼠10只为正常对照组。HPS各剂量组分别给予HPS 200,100,50 mg/kg,1次/d;依那普利10 mg/kg,1次/d;糖尿病模型组和正常对照组给予等剂量生理盐水,1次/d。灌胃给药8周,观察一般情况。采用实时定量荧光聚合酶链反应检测视网膜VEGF mRNA的相对表达量,免疫组织化学法观察小鼠视网膜VEGF蛋白的表达水平。结果正常对照组小鼠视网膜VEGF免疫阳性反应主要见于神经节细胞层及内丛状层,内核层少有表达。HPS各剂量组、依那普利组和糖尿病模型组小鼠视网膜VEGF表达阳性反应增强,视网膜各层细胞的胞质中均可见棕色的阳性颗粒,阳性反应部位主要位于神经节细胞层、内核层及内外丛状层。与正常对照组小鼠比较,糖尿病模型组小鼠视网膜VEGF蛋白表达和VEGF mRNA相对表达量均升高(P<0.01)。经HPS干预后,FIPS各剂量组VEGF蛋白表达和VEGFmRNA相对表达量均低于糖尿病模型组(尸<0.01)。结论 HPS可有效抑制db/db小鼠视网膜VEGF基因表达和蛋白合成,这可能是其治疗糖尿病视网膜病变的机制之一。Objective To study the influence of hedysarum polybotrys polysacchcaide (HPS) on the expression of vascular endothelial growth factor (VEGF) on db/db mice. Methods 50 db/db mice were randomly divided into five groups: model group (saline), enalaprilat group (10 mg/kg, once a day group), HPS (200 mg/kg, 100 mg/kg, 50 mg/kg, once a day group), normal group (saline). The mice were administrated by gavage for 8 weeks. The mRNA level and protein expressions of retinal VEGF were detected by using real-time PCR and Western blot method respectively. Results The expression of retinal VEGF was mainly found at Ganglion cell layer and inner plexiform layer, seldom at kernel layer in noral control mice. In HPS group with different dosage, enalapril group and diabetic model mice, visible brown positive particles were observed in the cytoplasm of cells of each layer of retina, primarily located at kernel layer and the inner and outer plexiform layer. Compared with the normal group, the mRNA level and protein expressions of retinal VEGF were increased in diabetic model mice (P 〈 0.05), HPS at different dosage could significantly decreas the the expression of retinal VEGF( P 〈 0.05). Conclusion HPS can effectively inhibit the expression of VEGF gene and protein synthesis in db/db mice, which may be one of the mechanisms for the treatment of diabetic retinopathy.
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