原创力文档azelnidipine prevents cardiac dysfunction in streptozotocin-diabetic rats by reducing intracellular calcium accumulation, oxidative stress and apoptosisazelnidipine防止心脏功能障碍在streptozotocin-diabetic老鼠通过减少细胞内钙积累,氧化应激和细胞凋亡.pdfVIP
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azelnidipine prevents cardiac dysfunction in streptozotocin-diabetic rats by reducing intracellular calcium accumulation, oxidative stress and apoptosisazelnidipine防止心脏功能障碍在streptozotocin-diabetic老鼠通过减少细胞内钙积累,氧化应激和细胞凋亡
Kain et al. Cardiovascular Diabetology 2011, 10:97 CARDIO
/content/10/1/97 VASCULAR
DIABETOLOGY
ORIGINAL INVESTIGATION Open Access
Azelnidipine prevents cardiac dysfunction in
streptozotocin-diabetic rats by reducing
intracellular calcium accumulation, oxidative
stress and apoptosis
† † *
Vasundhara Kain , Sandeep Kumar and Sandhya L Sitasawad
Abstract
Background: Numerous evidences suggest that diabetic heart is characterized by compromised ventricular
contraction and prolonged relaxation attributable to multiple causative factors including calcium accumulation,
oxidative stress and apoptosis. Therapeutic interventions to prevent calcium accumulation and oxidative stress
could be therefore helpful in improving the cardiac function under diabetic condition.
Methods: This study was designed to examine the effect of long-acting calcium channel blocker (CCB),
Azelnidipine (AZL) on contractile dysfunction, intracellular calcium (Ca2+) cycling proteins, stress-activated signaling
molecules and apoptosis on cardiomyocytes in diabetes. Adult male Wistar rats were made diabetic by a single
intraperitoneal (IP) injection of streptozotocin (STZ). Contractile functions were traced from live diabetic rats to
isolated individual cardiomyocytes including peak shortening (PS), time-to-PS (TPS), time-to-relengthening (TR90),
maximal velocity of shortening/relengthening (± dL/dt) and intracellular Ca2+ fluorescence.
Results: Diabetic heart showed significantly depressed PS, ± dL/dt, pro
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