论文部分内容阅读
目的 探讨黄精多糖对老年糖尿病小鼠脑组织糖基化终产物受体mRNA (RAGEmRNA)表达的调节作用。 方法 BALB/C小鼠 30只 ,随机分为对照组、糖尿病模型组和治疗组 ,每组 1 0只 ;糖尿病模型组和治疗组腹腔注射链脲佐菌素建立小鼠糖尿病模型 ,治疗组给予黄精多糖2ml/kg ,每日 1次灌胃给药 ,共 1 2周。各组实验动物脑组织RAGEmRNA表达的测定采用RT PCR法。 结果 糖尿病模型组实验鼠脑组织RAGEmRNA表达增加 ,RAGE/ β actin相对值 (0 1 5 3±0 0 5 4 )明显高于对照组 (0 ,P <0 0 1 )。应用黄精多糖治疗后 ,治疗组鼠脑组织RAGEmRNA表达较模型组降低 ,RAGE/ β actin相对值 (0 0 92± 0 0 33)显著低于模型组 (P <0 0 5 )。 结论 黄精多糖能抑制老年糖尿病鼠脑组织RAGEmRNA表达 ,对高血糖及糖基化终产物 (AGE)造成的脑组织损伤具有保护作用
Objective To investigate the regulatory effect of Polygonatum Polysaccharide (RPS) on the expression of RAGE mRNA in the brain of aged diabetic mice. Methods Thirty BALB / C mice were randomly divided into control group, diabetic model group and treatment group, with 10 rats in each group. Diabetic model group and treatment group were given diabetic model by intraperitoneal injection of streptozotocin, Polygonatum polysaccharide 2ml / kg, once daily oral administration, a total of 12 weeks. RAGEmRNA expression in brain tissue of experimental animals was determined by RT PCR method. Results The expression of RAGEmRNA in the brain tissue of diabetic rats increased, and the relative value of RAGE / β actin (0 1 53 ± 0 054) was significantly higher than that of the control group (0, P 0 01). After treated with Polygonatum Polysaccharide, the expression of RAGEmRNA in the treated group was lower than that in the untreated group, and the relative value of RAGE / β actin (0 0 92 ± 0 0 33) was significantly lower than that of the model group (P 0 05). Conclusion Polygonatum polysaccharide can inhibit the expression of RAGEmRNA in the brain tissue of senile diabetic rats and protect the brain tissue induced by hyperglycemia and advanced glycation end products (AGE)