消渴方对糖尿病大鼠糖脂代谢和肝肾损伤的影响

Effect of Diabetes Recipe on Glycolipid Metabolism and Hepatorenal Damage for STZ Induced Diabetic Rats

目的:从病理生理学的角度探讨消渴方对链脲佐菌素(STZ)诱导的糖尿病(DM)大鼠糖脂代谢、肝肾损伤的影响。方法:将SD大鼠随机分为4组,正常对照组、模型组、消渴方组及格列本脲组,每组8只。消渴方组及格列本脲组大鼠依次予消渴方(Diabetes Decoction,DD)及格列本脲(Glibenclamide,Glib)干预5周。期间监测各组大鼠体重(BW)、空腹血糖(FPG),血脂(甘油三酯(TG)、总胆固醇(TC)、肝功能指标(谷草氨基转移酶(AST)、谷丙氨基转移酶(ALT)、肾功能指标(肌酐(SCr)、尿素氮(BUN),光镜下观察各组大鼠胰腺、肝脏组织结构病理学改变。结果:模型组大鼠FPG、血脂、肝功能指标、肾功能指标均较正常组显著升高(P<0.01)。DD组及Glib组FPG、肝功能指标、肾功能指标水平较模型组显著降低(P<0.05),DD组血脂水平较Glib组、模型组显著降低(P<0.05),Glib组血脂水平较模型组差异无统计学意义(P>0.05)。结论:与格列本脲相比,消渴方可显著改善STZ诱导的糖尿病大鼠糖脂代谢紊乱,减轻肝肾损伤,其机制可能与促进胰岛β细胞再分化、促进胰岛素分泌、改善糖脂代谢有关,但具体作用机制尚不明确,有待进一步深入研究。

Objective:The effect of Diabetes Recipe on glycolipid metabolism and hepatorenal damage for rats with diabetes induced by streptozotocin(STZ)was assessed using histopathology.Methods:SD male rats were randomly divided into four groups of eight rats each.The normal controlled(NC)group was untreated.The diabetes controlled(DC)group was treated with STZ to induce diabetes.The Diabetes Recipe group(DR)was treated with STZ,then with Diabetes Recipe daily for 5 weeks.The glibenclamide(DFE)group was treated with STZ,then glibenclamide daily for 5 weeks.Body weight(BW),fasting blood glucose(FPG),blood lipid(TG,TC),liver function(AST,ALT),kidney function(SCR,BUN),histopathological changes of pancreas,liver and kidney were monitored during the experiment.Results:FPG,blood lipid,liver function index and renal function index in the model group were significantly higher than those in the normal controlled group(P<0.01).Compared with the model group,DD and glib could significantly reduce the levels of FPG,blood lipid,liver function index and renal function index of diabetes rats(P<0.05).Compared with the glib group and the model group,the blood lipid level of the DR group was significantly lower(P<0.05).There was no significant difference in blood lipid level between the glib group and the model group(P>0.05).Conclusion:Compared with Glib,DR can significantly improve glycolipid metabolism and reduce lhepatorenal damage in STZ induced diabetic rats.The mechanism may be related to the promotion the re-differentiation of beta cells,promotion of insulin secretion and improvement of glycolipid metabolism in the body,but the specific mechanism is still unclear and needs further study.