复方桑椹三七对链脲霉素糖尿病小鼠血糖与胰岛病理的影响

目的研究复方桑椹三七（CMN）对链脲霉素致糖尿病小鼠血糖与胰岛病理的影响。方法取雄性昆明（KM）小鼠,用链脲霉素（STZ）（150mg/kg）腹腔注射造模,选取血糖值在11～25mmol/L小鼠50只,随机分为模型组,阳性组（格列苯脲5mg/kg）,CMN高、中、低（9.0,3.0,1.5g/kg）剂量组（n=10）,另取10只未造模小鼠为正常对照组。灌胃给药30d,测定小鼠饮食、体质量、血糖、血清胰岛素水平,并将小鼠胰岛β细胞免疫染色,观察其病理变化。结果 CMN对糖尿病小鼠摄食量、排尿量、饮水量、空腹血糖与胰岛素水平的影响与模型组比较差异有统计学意义（P〈0.01或P〈0.05）;病理切片显示CMN可使小鼠胰岛β细胞免疫染色阳性数量明显增加,病理损伤明显好转,具体数据为,摄食量：正常组为（5.13±0.67）、模型组为（8.91±0.81）、格列苯脲组为（6.6±0.83）、CMN高剂量组为（4.56±0.89）、CMN中剂量组为（6.63±0.49）、CMN低剂量组为（8.26±0.92）;饮水量：正常组为（6.21±0.59）、模型组为（21.95±5.58）、格列苯脲组为（13.13±1.73）、CMN高剂量组为（10.19±2.00）、CMN中剂量组为（13.45±2.82）、CMN低剂量组为（16.80±5.68）;排尿量：正常组为（4.17±0.49）、模型组为（20.31±4.97）、格列苯脲组为（11.38±1.98）、CMN高剂量组为（9.63±2.13）、CMN中剂量组为（12.49±2.79）、CMN低剂量组为（15.53±5.66）;空腹血糖（第30天）：正常组为（4.91±0.89）、模型组为（20.58±6.69）、格列苯脲组为（12.71±6.60）、CMN高剂量组为（11.73±3.55）、CMN中剂量组为（12.52±6.78）、CMN低剂量组为（14.28±5.57）;血清胰岛素水平：正常组为（10.12±1.27）、模型组为（4.68±1.29）、格列苯脲组为（6.80±1.54）、CMN为高剂量组（6.23±1.62）、CMN中剂量组为（5.93±1.12）、CMN低剂量组为（5.72±0.97）;胰岛病理评分：正常组为（2.90±0.54）、模型组为（1.00±0.82）、格列苯脲组为（2.00±0.77）、CMN高剂量组为（2.40±0.49）、CMN中剂量组为（2.10±0.83）、CMN低剂量组为（1.90±0.54）。结论 CMN对糖尿病小鼠摄食量、饮水量、排尿量及空腹血糖具有明显降低作用,这可能与其保护修复胰岛β细胞,恢复胰岛素的分泌水平相关。

Objective To study the effects of Compound mulberry fruit notoginseng （CMN） on blood glucose and islet pathology in streptozotocin（STZ）-induced diabetic mice. Methods Kunming mice, SPF, male, were adopted in this test. Diabetic mouse model was induced by STZ （150 mg/kg）, given by intraperitoneal injection. 50 mice, whose blood glucose ranged from 11-25 mmol/L, were randomly divided in to 5 groups, such as model group, glibenclamide group（5 mg/kg） and CMN high-, middle-, low-dose group（9.0,3.0,1.5 g/kg）. Another ten normal mice were taken as control group. After administration for 30 days, diet, voided volume, weight, insulin levels, and fasting blood glucose of the mice were observed, and pancreaticβcells were immuno-stained for pathological observation. Results The results showed that there were significant difference （P＆lt;0.01 or P＆lt;0.05） in food, water intake, voided volume, insulin levels, and fasting plasma glucose between drug group and model group. Pathological sections showed that CMN increased positive immuno-stained pancreaticβcells, and the pathological lesions improved markedly, With data,Food intake：Normal group is （5.13±0.67）, Model group is （8.91±0.81）, Glibenclamide group is （6.6±0.83）, CMN high dose group is （4.56±0.89）, CMN medium dose group is （6.63±0.49）, CMN low dose group is （8.26±0.92）;Water intake：Normal group is （6.21±0.59）, Model group is （21.95±5.58）, Glibenclamide group is （13.13±1.73）, CMN high dose group is （10.19±2.00）, CMN medium dose group is （13.45±2.82）, CMN low dose group is （16.80±5.68）;The quantity of urine：Normal group is （4.17±0.49） , Model group is （20.31±4.97）, Glibenclamide group is （11.38±1.98）, CMN high dose group is （9.63±2.13）, CMN medium dose group is （12.49±2.79）, CMN low dose group is （15.53±5.66）;Fasting blood glucose （30 th days）：Normal group is （4.91±0.89, Model group is （20.58±6.69）, Glibenclamide group is （12.71±6.60）, CMN high dose group is （11.73±3.55）, CMN medium dose group is （12.52±6.78）, CMN low dose group is （14.28±5.57）;The serum level of insulin：Normal group is （10.12±1.27）, Model group is （4.68±1.29）, Glibenclamide group is （6.80±1.54）, CMN high dose group is （6.23±1.62）, CMN medium dose group is （5.93±1.12）, CMN low dose group is （5.72±0.97）;Islet pathology score：Normal group is （2.90±0.54）, Model group is （1.00±0.82）, Glibenclamide group is （2.00±0.77）, CMN high dose group is （2.40±0.49）, CMN medium dose group is （2.10±0.83）, CMN low dose group is （1.90±0.54）. Conclusion CMN significantly reduces food, water intake, voided volume, insulin levels, and fasting plasma glucose on STZ-induced diabetic mice. This may be ascribe to its function of protecting the pancreaticβcells and restore the insulin secretion.