| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Division of Pharmaceutical Sciences and Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie, WY, USA
* To whom correspondence should be addressed. E-mail: jren{at}uwyo.edu.
Diabetic cardiomyopathy is characterized by cardiac dysfunction. This study was designed to examine the effect of benfotiamine, a lipophilic derivative of thiamine, on streptozotocin (STZ)-induced cardiac contractile dysfunction in mouse cardiomyocytes. Adult male FVB mice were made diabetic with a single injection of STZ (200 mg/kg, i.p.). Fourteen days later, control and diabetic (fasting plasma glucose > 13.9 mM) mice were put on benfotiamine therapy (100 mg/kg/d, i.p.) for another 14 days. Mechanical and intracellular Ca2+ properties were evaluated in left ventricular myocytes using an IonOptix MyoCam system. The following indices were evaluated: peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR90), maximal velocity of shortening/relengthening (± dL/dt), resting and rise of intracellular Ca2+ in response to electrical stimulus, sarcoplasmic reticulum (SR) Ca2+ load and intracellular Ca2+ decay rate (tau). Two or 4 weeks STZ treatment led to hyperglycemia, prolonged TPS and TR90, reduced SR Ca2+-load, elevated resting intracellular Ca2+ level and prolonged tau associated with normal PS, ± dL/dt and intracellular Ca2+ rise in response to electrical stimulus. Benfotiamine treatment abolished prolongation in TPS, TR90 and tau as well as reduction in SR Ca2+ load without affecting hyperglycemia and elevated resting intracellular Ca2+. Diabetes triggered oxidative stress, measured by GSH/GSSG ratio and formation of advanced glycation end-product (AGE) in the hearts. Benfotiamine treatment alleviated oxidative stress without affecting AGE or protein carbonyl formation. Collectively, our results indicated benfotiamine may rescue STZ-induced cardiomyocyte dysfunction but unlikely AGE formation in short-term diabetes.
This article has been cited by other articles:
|
|
 |
|
  N. Mariappan, C. M. Elks, S. Sriramula, A. Guggilam, Z. Liu, O. Borkhsenious, and J. Francis NF-{kappa}B-induced oxidative stress contributes to mitochondrial and cardiac dysfunction in type II diabetes Cardiovasc Res, September 25, 2009; (2009) cvp305v2. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Bugger and E. D. Abel Rodent models of diabetic cardiomyopathy Dis. Model. Mech., September 1, 2009; 2(9-10): 454 - 466. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Q. Li, L. K. Hueckstaedt, and J. Ren The protease inhibitor UCF-101 ameliorates streptozotocin-induced mouse cardiomyocyte contractile dysfunction in vitro: role of AMP-activated protein kinase Exp Physiol, September 1, 2009; 94(9): 984 - 994. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Han, R. Baliga, H. Huang, P. J. Giannone, and J. A. Bauer Decreased cardiac expression of vascular endothelial growth factor and redox imbalance in murine diabetic cardiomyopathy Am J Physiol Heart Circ Physiol, August 1, 2009; 297(2): H829 - H835. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Tikellis, M. C. Thomas, B. E. Harcourt, M. T. Coughlan, J. Pete, K. Bialkowski, A. Tan, A. Bierhaus, M. E. Cooper, and J. M. Forbes Cardiac inflammation associated with a Western diet is mediated via activation of RAGE by AGEs Am J Physiol Endocrinol Metab, August 1, 2008; 295(2): E323 - E330. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. J. Crespo, J. Zalacain, D. C. Dunbar, N. Cruz, and L. Arocho Cardiac Oxidative Stress Is Elevated at the Onset of Dilated Cardiomyopathy in Streptozotocin-Diabetic Rats Journal of Cardiovascular Pharmacology and Therapeutics, March 1, 2008; 13(1): 64 - 71. [Abstract] [PDF]
|
|
|
|
 |
|
 W. Hsueh, E. D. Abel, J. L. Breslow, N. Maeda, R. C. Davis, E. A. Fisher, H. Dansky, D. A. McClain, R. McIndoe, M. K. Wassef, et al. Recipes for Creating Animal Models of Diabetic Cardiovascular Disease Circ. Res., May 25, 2007; 100(10): 1415 - 1427. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Boudina and E. D. Abel Mitochondrial uncoupling: a key contributor to reduced cardiac efficiency in diabetes. Physiology, August 1, 2006; 21: 250 - 258. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. Marchetti, R. Menghini, S. Rizza, A. Vivanti, T. Feccia, D. Lauro, A. Fukamizu, R. Lauro, and M. Federici Benfotiamine Counteracts Glucose Toxicity Effects on Endothelial Progenitor Cell Differentiation via Akt/FoxO Signaling. Diabetes, August 1, 2006; 55(8): 2231 - 2237. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
