当代医学
噹代醫學
당대의학
CHINA CONTEMPORARY MEDICINE
2014年
29期
6-8
,共3页
杜正彩%邓家刚%黄庆%庞国凤%李好文
杜正綵%鄧傢剛%黃慶%龐國鳳%李好文
두정채%산가강%황경%방국봉%리호문
桑椹%三七%小鼠%链脲霉素%糖尿病
桑椹%三七%小鼠%鏈脲黴素%糖尿病
상심%삼칠%소서%련뇨매소%당뇨병
Mulberry fruit%Notoginseng%Mouse%Streptozotocin%Diabetes
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)(150 mg/kg)腹腔注射造模,选取血糖值在11~25 mmol/L小鼠50只,随机分为模型组,阳性组(格列苯脲5 mg/kg),CMN高、中、低(9.0,3.0,1.5 g/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30 d,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。
目的:研究複方桑椹三七(CMN)對鏈脲黴素緻糖尿病小鼠血糖與胰島病理的影響。方法取雄性昆明(KM)小鼠,用鏈脲黴素(STZ)(150 mg/kg)腹腔註射造模,選取血糖值在11~25 mmol/L小鼠50隻,隨機分為模型組,暘性組(格列苯脲5 mg/kg),CMN高、中、低(9.0,3.0,1.5 g/kg)劑量組(n=10),另取10隻未造模小鼠為正常對照組。灌胃給藥30 d,測定小鼠飲食、體質量、血糖、血清胰島素水平,併將小鼠胰島β細胞免疫染色,觀察其病理變化。結果 CMN對糖尿病小鼠攝食量、排尿量、飲水量、空腹血糖與胰島素水平的影響與模型組比較差異有統計學意義(P<0.01或P<0.05);病理切片顯示CMN可使小鼠胰島β細胞免疫染色暘性數量明顯增加,病理損傷明顯好轉,具體數據為,攝食量:正常組為(5.13±0.67)、模型組為(8.91±0.81)、格列苯脲組為(6.6±0.83)、CMN高劑量組為(4.56±0.89)、CMN中劑量組為(6.63±0.49)、CMN低劑量組為(8.26±0.92);飲水量:正常組為(6.21±0.59)、模型組為(21.95±5.58)、格列苯脲組為(13.13±1.73)、CMN高劑量組為(10.19±2.00)、CMN中劑量組為(13.45±2.82)、CMN低劑量組為(16.80±5.68);排尿量:正常組為(4.17±0.49)、模型組為(20.31±4.97)、格列苯脲組為(11.38±1.98)、CMN高劑量組為(9.63±2.13)、CMN中劑量組為(12.49±2.79)、CMN低劑量組為(15.53±5.66);空腹血糖(第30天):正常組為(4.91±0.89)、模型組為(20.58±6.69)、格列苯脲組為(12.71±6.60)、CMN高劑量組為(11.73±3.55)、CMN中劑量組為(12.52±6.78)、CMN低劑量組為(14.28±5.57);血清胰島素水平:正常組為(10.12±1.27)、模型組為(4.68±1.29)、格列苯脲組為(6.80±1.54)、CMN為高劑量組(6.23±1.62)、CMN中劑量組為(5.93±1.12)、CMN低劑量組為(5.72±0.97);胰島病理評分:正常組為(2.90±0.54)、模型組為(1.00±0.82)、格列苯脲組為(2.00±0.77)、CMN高劑量組為(2.40±0.49)、CMN中劑量組為(2.10±0.83)、CMN低劑量組為(1.90±0.54)。結論 CMN對糖尿病小鼠攝食量、飲水量、排尿量及空腹血糖具有明顯降低作用,這可能與其保護脩複胰島β細胞,恢複胰島素的分泌水平相關。
목적:연구복방상심삼칠(CMN)대련뇨매소치당뇨병소서혈당여이도병리적영향。방법취웅성곤명(KM)소서,용련뇨매소(STZ)(150 mg/kg)복강주사조모,선취혈당치재11~25 mmol/L소서50지,수궤분위모형조,양성조(격렬분뇨5 mg/kg),CMN고、중、저(9.0,3.0,1.5 g/kg)제량조(n=10),령취10지미조모소서위정상대조조。관위급약30 d,측정소서음식、체질량、혈당、혈청이도소수평,병장소서이도β세포면역염색,관찰기병리변화。결과 CMN대당뇨병소서섭식량、배뇨량、음수량、공복혈당여이도소수평적영향여모형조비교차이유통계학의의(P<0.01혹P<0.05);병리절편현시CMN가사소서이도β세포면역염색양성수량명현증가,병리손상명현호전,구체수거위,섭식량:정상조위(5.13±0.67)、모형조위(8.91±0.81)、격렬분뇨조위(6.6±0.83)、CMN고제량조위(4.56±0.89)、CMN중제량조위(6.63±0.49)、CMN저제량조위(8.26±0.92);음수량:정상조위(6.21±0.59)、모형조위(21.95±5.58)、격렬분뇨조위(13.13±1.73)、CMN고제량조위(10.19±2.00)、CMN중제량조위(13.45±2.82)、CMN저제량조위(16.80±5.68);배뇨량:정상조위(4.17±0.49)、모형조위(20.31±4.97)、격렬분뇨조위(11.38±1.98)、CMN고제량조위(9.63±2.13)、CMN중제량조위(12.49±2.79)、CMN저제량조위(15.53±5.66);공복혈당(제30천):정상조위(4.91±0.89)、모형조위(20.58±6.69)、격렬분뇨조위(12.71±6.60)、CMN고제량조위(11.73±3.55)、CMN중제량조위(12.52±6.78)、CMN저제량조위(14.28±5.57);혈청이도소수평:정상조위(10.12±1.27)、모형조위(4.68±1.29)、격렬분뇨조위(6.80±1.54)、CMN위고제량조(6.23±1.62)、CMN중제량조위(5.93±1.12)、CMN저제량조위(5.72±0.97);이도병리평분:정상조위(2.90±0.54)、모형조위(1.00±0.82)、격렬분뇨조위(2.00±0.77)、CMN고제량조위(2.40±0.49)、CMN중제량조위(2.10±0.83)、CMN저제량조위(1.90±0.54)。결론 CMN대당뇨병소서섭식량、음수량、배뇨량급공복혈당구유명현강저작용,저가능여기보호수복이도β세포,회복이도소적분비수평상관。
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<0.01 or P<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.