中国肝脏病杂志（电子版）
中國肝髒病雜誌（電子版）
중국간장병잡지（전자판）
CHINESE JOURNAL OF LIVER DISEASES(ELECTRONIC VERSION)
2015年
1期
55-58
,共4页
张霞%雷飞飞%李芳%谭华炳
張霞%雷飛飛%李芳%譚華炳
장하%뢰비비%리방%담화병
2型糖尿病合并非酒精性脂肪性肝病%绞股蓝提取物和银杏叶提取物混合物%脂肪肝程度%影响%动物
2型糖尿病閤併非酒精性脂肪性肝病%絞股藍提取物和銀杏葉提取物混閤物%脂肪肝程度%影響%動物
2형당뇨병합병비주정성지방성간병%교고람제취물화은행협제취물혼합물%지방간정도%영향%동물
T2DM and nonalcoholic fatty liver disease%GPS and GBE mixture%Degree of fatty liver disease%Inlfuence%Animal
目的：观察绞股蓝皂苷（GPS）和银杏叶提取物（GBE）混合物对2型糖尿病（T2DM）合并非酒精性脂肪性肝病（NAFLD）大鼠脂肪肝程度的影响。方法40只SPF级雄性SD大鼠随机分为空白组、T2DM合并NAFLD模型组，造模周期8周。将T2DM合并NAFLD模型随机分为模型组（给予同等体积的纯净水灌胃）、对照组[给予GPS 0.5 g/（kg·d）灌胃]、治疗组[给予GPS 0.5 g/（kg·d）加GBE 0.1 g/（kg·d）灌胃]。继续予高糖高脂饲料，自由饮水；治疗周期为6周；实验周期14周。检测血糖（BS）、甘油三酯（TG）、总胆固醇（TC）、ALT、AST。检测肝组织TG及肝脏病理学。结果空白组、模型组、治疗组、对照组BS水平分别为（5.50±0.51）mmol/L、（18.76±4.20）mmol/L、（10.78±3.38）mmol/L、（14.62±3.32）mmol/L，治疗组、对照组低于模型组（P＜0.01），治疗组低于对照组（P＜0.01）。空白组、模型组、治疗组、对照组TG水平分别为（0.81±0.11）mmol/L、（1.29±0.14）mmol/L、（0.90±0.09）mmol/L、（1.09±0.10）mmol/L，治疗组、对照组低于模型组（P＜0.01），治疗组低于对照组（P＜0.05）。空白组、模型组、治疗组、对照组TC水平分别为（1.39±0.13）mmol/L、（3.69±0.27）mmol/L、（2.59±0.19）mmol/L、（3.11±0.18）mmol/L，治疗组、对照组低于模型组（P均＜0.01），治疗组低于对照组（P＜0.01）。空白组、模型组、治疗组、对照组ALT水平分别为（35.12±3.34）U/L、（60.68±5.12）U/L、（42.13±4.99）U/L、（50.12±4.68）U/L，治疗组、对照组低于模型组（P均＜0.01），治疗组低于对照组（P＜0.05）。空白组、模型组、治疗组、对照组AST水平分别为（81.15±7.14）U/L、（168.12±10.49）U/L、（112.23±10.12）U/L、（139.12±11.68）U/L，治疗组、对照组低于模型组（P＜0.01），治疗组低于对照组（P＜0.01）。空白组、模型组、治疗组、对照组肝组织TG水平分别为（30.26±2.48）mg/G、（228.46±8.48）mg/G、（153.12±9.98）mg/G、（196.24±9.78）mg/G，治疗组、对照组低于模型组（P＜0.05），治疗组低于对照组（P＜0.01）。空白组为正常肝组织，模型组为重度脂肪肝，治疗组和对照组为中-重度脂肪肝，脂肪肝程度治疗组轻于对照组。结论 GPS和GBE混合物通过调整血糖、脂质代谢，减少肝组织TG沉积，保护肝细胞，达到降低T2DM合并NAFLD大鼠模型脂肪肝程度的目的。
目的：觀察絞股藍皂苷（GPS）和銀杏葉提取物（GBE）混閤物對2型糖尿病（T2DM）閤併非酒精性脂肪性肝病（NAFLD）大鼠脂肪肝程度的影響。方法40隻SPF級雄性SD大鼠隨機分為空白組、T2DM閤併NAFLD模型組，造模週期8週。將T2DM閤併NAFLD模型隨機分為模型組（給予同等體積的純淨水灌胃）、對照組[給予GPS 0.5 g/（kg·d）灌胃]、治療組[給予GPS 0.5 g/（kg·d）加GBE 0.1 g/（kg·d）灌胃]。繼續予高糖高脂飼料，自由飲水；治療週期為6週；實驗週期14週。檢測血糖（BS）、甘油三酯（TG）、總膽固醇（TC）、ALT、AST。檢測肝組織TG及肝髒病理學。結果空白組、模型組、治療組、對照組BS水平分彆為（5.50±0.51）mmol/L、（18.76±4.20）mmol/L、（10.78±3.38）mmol/L、（14.62±3.32）mmol/L，治療組、對照組低于模型組（P＜0.01），治療組低于對照組（P＜0.01）。空白組、模型組、治療組、對照組TG水平分彆為（0.81±0.11）mmol/L、（1.29±0.14）mmol/L、（0.90±0.09）mmol/L、（1.09±0.10）mmol/L，治療組、對照組低于模型組（P＜0.01），治療組低于對照組（P＜0.05）。空白組、模型組、治療組、對照組TC水平分彆為（1.39±0.13）mmol/L、（3.69±0.27）mmol/L、（2.59±0.19）mmol/L、（3.11±0.18）mmol/L，治療組、對照組低于模型組（P均＜0.01），治療組低于對照組（P＜0.01）。空白組、模型組、治療組、對照組ALT水平分彆為（35.12±3.34）U/L、（60.68±5.12）U/L、（42.13±4.99）U/L、（50.12±4.68）U/L，治療組、對照組低于模型組（P均＜0.01），治療組低于對照組（P＜0.05）。空白組、模型組、治療組、對照組AST水平分彆為（81.15±7.14）U/L、（168.12±10.49）U/L、（112.23±10.12）U/L、（139.12±11.68）U/L，治療組、對照組低于模型組（P＜0.01），治療組低于對照組（P＜0.01）。空白組、模型組、治療組、對照組肝組織TG水平分彆為（30.26±2.48）mg/G、（228.46±8.48）mg/G、（153.12±9.98）mg/G、（196.24±9.78）mg/G，治療組、對照組低于模型組（P＜0.05），治療組低于對照組（P＜0.01）。空白組為正常肝組織，模型組為重度脂肪肝，治療組和對照組為中-重度脂肪肝，脂肪肝程度治療組輕于對照組。結論 GPS和GBE混閤物通過調整血糖、脂質代謝，減少肝組織TG沉積，保護肝細胞，達到降低T2DM閤併NAFLD大鼠模型脂肪肝程度的目的。
목적：관찰교고람조감（GPS）화은행협제취물（GBE）혼합물대2형당뇨병（T2DM）합병비주정성지방성간병（NAFLD）대서지방간정도적영향。방법40지SPF급웅성SD대서수궤분위공백조、T2DM합병NAFLD모형조，조모주기8주。장T2DM합병NAFLD모형수궤분위모형조（급여동등체적적순정수관위）、대조조[급여GPS 0.5 g/（kg·d）관위]、치료조[급여GPS 0.5 g/（kg·d）가GBE 0.1 g/（kg·d）관위]。계속여고당고지사료，자유음수；치료주기위6주；실험주기14주。검측혈당（BS）、감유삼지（TG）、총담고순（TC）、ALT、AST。검측간조직TG급간장병이학。결과공백조、모형조、치료조、대조조BS수평분별위（5.50±0.51）mmol/L、（18.76±4.20）mmol/L、（10.78±3.38）mmol/L、（14.62±3.32）mmol/L，치료조、대조조저우모형조（P＜0.01），치료조저우대조조（P＜0.01）。공백조、모형조、치료조、대조조TG수평분별위（0.81±0.11）mmol/L、（1.29±0.14）mmol/L、（0.90±0.09）mmol/L、（1.09±0.10）mmol/L，치료조、대조조저우모형조（P＜0.01），치료조저우대조조（P＜0.05）。공백조、모형조、치료조、대조조TC수평분별위（1.39±0.13）mmol/L、（3.69±0.27）mmol/L、（2.59±0.19）mmol/L、（3.11±0.18）mmol/L，치료조、대조조저우모형조（P균＜0.01），치료조저우대조조（P＜0.01）。공백조、모형조、치료조、대조조ALT수평분별위（35.12±3.34）U/L、（60.68±5.12）U/L、（42.13±4.99）U/L、（50.12±4.68）U/L，치료조、대조조저우모형조（P균＜0.01），치료조저우대조조（P＜0.05）。공백조、모형조、치료조、대조조AST수평분별위（81.15±7.14）U/L、（168.12±10.49）U/L、（112.23±10.12）U/L、（139.12±11.68）U/L，치료조、대조조저우모형조（P＜0.01），치료조저우대조조（P＜0.01）。공백조、모형조、치료조、대조조간조직TG수평분별위（30.26±2.48）mg/G、（228.46±8.48）mg/G、（153.12±9.98）mg/G、（196.24±9.78）mg/G，치료조、대조조저우모형조（P＜0.05），치료조저우대조조（P＜0.01）。공백조위정상간조직，모형조위중도지방간，치료조화대조조위중-중도지방간，지방간정도치료조경우대조조。결론 GPS화GBE혼합물통과조정혈당、지질대사，감소간조직TG침적，보호간세포，체도강저T2DM합병NAFLD대서모형지방간정도적목적。
Objective To observe effect of the degrees of fatty liver disease in rat with type 2 diabetes mellitus and nonalcoholic fatty liver disease was inhibited by Gypenosides and Ginkgo Biloba Extract Mixture.Methods Total of 40 SPF male SD rats, body mass 220-250 g, were randomly divided into blank control group, model group with type two diabetes mellitus and nonalcoholic fatty liver disease. After eight weeks the NAFLD model in rats was maked, model group were divided into three groups: treatment group were perfused with 500 mg/(kg·d) GPS and 0.1g/(kg·d) ginkgo biloba extract mixture, control group were perfused with 500 mg/(kg·d) GPS, model group were perfused with the same volume of water, and high fat diet at the same time, the experimental period was six weeks. The experimental period was 14 weeks. Blood sugar, triglycerides, total cholesterol (TC), ALT, AST in the plasma in rat was test. It was tested that triglycerides in the liver tissue. The Liver tissue was detected by pathology.Results BS levels in plasma: blank control group (5.50 ±0.51) mmol/L, model group (18.76 ±4.20) mmol/L, treatment group (10.78 ±3.389) mmol/L, control group (14.62 ±3.32) mmol/L, treatment group and control group was lower than model group, there was a signiifcant difference (P< 0.01),treatment group was lower than control group, there was a signiifcant difference (P< 0.05).TG levels in plasma: blank control group (0.81 ±0.11) mmol/L, model group (1.29 ±0.14) mmol/L, treatment group (0.90 ±0.09) mmol/L, control group (1.09 ± 0.10) mmol/L, treatment group and control group was lower than model group, there was a signiifcant difference (P< 0.01),treatment group was lower than and control group, there was a signiifcant difference (P< 0.05). TC levels in plasma: blank control group (1.39 ±0.13) mmol/L, model group (3.69 ±0.27) mmol/L, treatment group (2.59 ± 0.19) mmol/L, control group (3.11 ±0.18) mmol/L, treatment group and control group was lower than model group, there was a signiifcant difference (P< 0.05),treatment group was lower than control group (P< 0.05). ALT levels in plasma: blank control group (35.12 ±3.34) U/L, model group (60.68 ±5.12) U/L, treatment group (42.13 ±4.99) U/L, control group (50.12 ±4.68) U/L, treatment group and control group was lower than model group, there was a signiifcant difference (P< 0.05),treatment group was lower than control group (P< 0.05). AST levels in plasma: blank control group (81.15 ±7.14) U/L, model group (168.12 ±10.49) U/L, treatment group (112.23 ±10.12) U/L, control group (139.12 ±11.68) U/L, treatment group and control group was lower than model group (P< 0.01), treatment groupwas lower than control group (P< 0.01).TG levels in liver tisue: blank control group (30.26 ±2.48) mg/g, model group (228.46 ±8.48) mg/g, treatment group (153.12 ±9.98) mg/g, control group (196.24 ±9.78) mg/g, treatment group and control group was lower than model group, there was a signiifcant difference (P< 0.05),treatment group was lower than control group (P< 0.05). Liver pathology:blank control group was normal liver tissues. Model group was severe fatty liver disease. Treatment group and control group was moderate to severe fatty liver disease, and treatment group was lighter than control group.Conclusions The degree of T2DM and nonalcoholic fatty liver disease in rats was inhibited by gypenosides and ginkgo biloba extract mixture, through blood sugar and lipid metabolism adjusted, and reduce the liver tissue TG deposition, protecting liver cells.
