Impact of 1, 25-(OH)2D3 on Left Ventricular Hypertrophy in Type 2 Diabetic Rats / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the impact of 1, 25-(OH)2D3 on left ventricular hypertrophy (LVH) in type 2 diabetic rats.</p><p><b>METHODS</b>Type 2 diabetic mellitus (DM) model rats were established by intraperitoneally injecting with 30 mg/kg streptozotocin. After 8 weeks, 19 male rats were identified as diabetic with left ventricular hypertrophy (LVH) by ultrasound examination, and randomly assigned into three groups: untreated (DM-LVH, n=7), treated with insulin (DM-LVH+INS, n=6), and treated with 1, 25-(OH)2D3 (DM-LVH+VD, n=6). Healthy male rats were used as the controls group (n=6). The fasting blood glucose and the insulin level were determined weekly. The left ventricular mass index, myocardial collagen content, collagen volume fraction, and 1, 25-(OH)2D3-receptor level were determined by 4 weeks later.</p><p><b>RESULTS</b>In the DM-LVH model group, the insulin level was significantly decreased compared with the non-diabetic control group (P<0.05), whereas the blood glucose, left ventricular mass index, myocardial collagen content, collagen volume fraction, and 1, 25-(OH)2D3-receptor expression were significantly increased (all P<0.05). In the DM-LVH+INS and DM-LVH+VD groups, the insulin levels were significantly increased compared with the DM-LVH model group (P<0.05), whereas the other parameters were significantly decreased (all P<0.05).</p><p><b>CONCLUSION</b>1, 25-(OH)2D3 could reverse LVH in diabetic rats and that the mechanism may involve stimulating insulin secretion and reducing blood glucose via direct up-regulation of 1, 25-(OH)2D3-receptor expression.</p>

Effects of telmisartan on endoplasmic reticulum stress induced cardiomyocyte apoptosis in abdominal aortic banded rats / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the effects of telmisartan on endoplasm reticulum (ER) stress signal pathways and cardiomyocyte apoptosis in abdominal aortic banded rats.</p><p><b>METHODS</b>Male SD rats were randomly divided into sham-operated group, abdominal aortic banding group (AAB) and AAB + telmisartan (5 mgxkg(-1)xd(-1) per gavage, beginning at 1 week before AAB for 8 weeks, n = 10 each). Ten weeks post AAB, hemodynamic measurements were performed, whole heart and left ventricular weights were obtained, cardiomyocyte apoptosis was measured by TUNEL method. Myocardial GRP78 and CHOP protein expressions were detected by Western blot and immunohistochemistry.</p><p><b>RESULTS</b>The ratio of left ventricular weight to body weight, the ratio of heart weight to body weight, left ventricular end diastolic pressure and the apoptosis index were significantly increased while left ventricular end systolic pressure and +/- dp/dt(max) were significantly decreased in AAB group than those in sham-operated group (all P < 0.01), these changes could be significantly attenuated by telmisartan (all P < 0.01). Moreover, myocardial GRP78 and CHOP expressions were significantly upregulated in AAB group than those in sham-operated group and telmisartan could significantly downregulate the increased GRP78, CHOP expressions (all P < 0.01).</p><p><b>CONCLUSIONS</b>Increased ER stress might be responsible for enhanced cardiomyocyte apoptosis in AAB rats. Telmisartan effectively attenuated the cardiomyocyte apoptosis and cardiac hypertrophy in AAB rats possibly through reducing ER stress.</p>