HYPOGLYCAEMIC AND HYPOLIPIDAEMIC EFFECTS OF EMODIN AND ITS EFFECT ON L-TYPE CALCIUM CHANNELS IN DYSLIPIDAEMIC-DIABETIC RATS

被引:39
作者
Zhao, Xiao-Yan [1 ,2 ]
Qiao, Guo-Fen [1 ,2 ]
Li, Bao-Xin [1 ]
Chai, Li-Min [1 ]
Li, Zhe [1 ]
Lu, Yan-Jie [1 ,2 ]
Yang, Bao-Feng [1 ,2 ]
机构
[1] Harbin Med Univ, Dept Pharmacol, Harbin 150081, Peoples R China
[2] Harbin Med Univ, State Prov Key Labs Biomed Pharmaceut, Harbin 150081, Peoples R China
基金
中国国家自然科学基金;
关键词
diabetes mellitus; emodin; heart; islets of langerhans; L-type calcium channels; STREPTOZOTOCIN-TREATED RAT; BETA-CELL; INSULIN-SECRETION; CA2+ CHANNELS; CARDIOVASCULAR-DISEASE; MELLITUS; RESISTANCE; GLUCOSE; OBESITY; MODEL;
D O I
10.1111/j.1440-1681.2008.05051.x
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The aim of the present study was to evaluate the hypoglycaemic and hypolipidaemic effects of 20, 40 and 80 mg/kg per day emodin and its potential effects on L-type calcium channels in dyslipidaemic-diabetic rats. Dyslipidaemic-diabetic rats were induced by a single intraperitoneal injection of streptozotocin (55 mg/kg) after intragastric administration of a high-fat diet for 2 weeks. Daily administration of emodin for 2 weeks resulted in a significant dose-dependent reductions in blood glucose, serum total cholesterol, triglycerides, free fatty acids and malonaldehyde (P < 0.05) in dyslipidaemic-diabetic rats compared with vehicle-treated dyslipidaemic-diabetic rats. In addition, emodin caused dose-dependent increases in plasma superoxide dismutase activity in dyslipidaemic-diabetic rats (P < 0.05). Immunofluorescent staining and reverse transcription-polymerase chain reaction showed that the expression of L-type calcium channels in the pancreas and heart was restored, to different extents, by the three doses of emodin treatment. The results of the present study suggest that emodin has antidiabetic and lipid-modulating effects that involve, in part, upregulation of L-type calcium channel expression in the pancreas and heart in dyslipidaemic-diabetic rats.
引用
收藏
页码:29 / 34
页数:6
相关论文
共 37 条
[1]   Role of changes in cardiac metabolism in development of diabetic cardiomyopathy [J].
An, Ding ;
Rodrigues, Brian .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2006, 291 (04) :H1489-H1506
[2]   Cardiac excitation-contraction coupling [J].
Bers, DM .
NATURE, 2002, 415 (6868) :198-205
[3]   Free fatty acids in obesity and type 2 diabetes:: defining their role in the development of insulin resistance and β-cell dysfunction [J].
Boden, G ;
Shulman, GI .
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, 2002, 32 :14-23
[4]   Genotoxicity of Streptozotocin [J].
Bolzán, AD ;
Bianchi, MS .
MUTATION RESEARCH-REVIEWS IN MUTATION RESEARCH, 2002, 512 (2-3) :121-134
[5]   Structure and function of neuronal Ca2+ channels and their role in neurotransmitter release [J].
Catterall, WA .
CELL CALCIUM, 1998, 24 (5-6) :307-323
[6]   Long-term high-fat feeding leads to severe insulin resistance but not diabetes in Wistar rats [J].
Chalkley, SM ;
Hettiarachchi, M ;
Chisholm, DJ ;
Kraegen, EW .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2002, 282 (06) :E1231-E1238
[7]   Phasic insulin release and metabolic regulation in type 2 diabetes [J].
Del Prato, S ;
Marchetti, P ;
Bonadonna, RC .
DIABETES, 2002, 51 :S109-S116
[8]  
Dolphin AC, 1999, ADV SEC MESS PHOSPH, V33, P153
[9]   Glucose and palmitic acid induce degeneration of myofibrils and modulate apoptosis in rat adult cardiomyocytes [J].
Dyntar, D ;
Eppenberger-Eberhardt, M ;
Maedler, K ;
Pruschy, M ;
Eppenberger, HM ;
Spinas, GA ;
Donath, MY .
DIABETES, 2001, 50 (09) :2105-2113
[10]   A critical role for PPARα-mediated lipotoxicity in the pathogenesis of diabetic cardiomyopathy:: Modulation by dietary fat content [J].
Finck, BN ;
Han, XL ;
Courtois, M ;
Aimond, F ;
Nerbonne, JM ;
Kovacs, A ;
Gross, RW ;
Kelly, DP .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (03) :1226-1231