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Publications (5)1.52 Total impact

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    ABSTRACT: Vascular complications associated with diabetes are the major cause for the increased morbidity and mortality in diabetic patients. However, the progression of vascular complications in diabetes is not well understood. We aimed to investigate the biomechanical and biochemical changes associated with vascular dysfunction in diabetic rats. Male Wistar rats were randomly divided into two groups: normal control (n = 8) and fat-fed, streptozotocin-treated diabetic rats (n = 11). After 16 weeks, Peterson's modulus of elasticity (Ep) and cross-sectional distensibility (CD) were calculated and compared between the two groups. Aortas were harvested from rats for histopathological and electron-microscopic analysis. Collagenous fibers were scattered in the extracellular matrix and invaded the elastic lamina in the aortas of diabetic rats, suggesting a significant accumulation of collagen in diabetic vessels. Compared with normal rats, diabetic rats showed significantly reduced aortic distensibility (CD: 0.10 +/- 0.04 vs. 0.17 +/- 0.08 kPa(-1), p = 0.033) and an increased aortic stiffness index (Ep: 0.25 +/- 0.13 vs. 0.15 +/- 0.05 x 10(6) dyn/cm(2), p = 0.045). Ep was positively and CD negatively correlated with glucose and collagen in diabetic rats. In diabetic rats, elastic properties of the aorta are impaired, being closely related to hyperglycemia-induced vascular wall remodeling.
    Cardiology 06/2009; 114(2):107-13. · 1.52 Impact Factor
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    ABSTRACT: To study the activation of transforming growth factor (TGF)-beta(1)/Smads signal pathway in diabetic cardiomyopathy (DCM) and effects of valsartan thereon. 40 male Wistar rats were randomly divided into 3 groups: DCM group (n = 16, fed with high-calorie fat diet for 4 weeks, injected intraperitoneally with streptozocin so as to establish DCM model, and then perfused into the stomach with normal saline once daily since the injection of STZ for 16 weeks), valsartan group (n = 16, perfused into the stomach with valsartan at the dose of 30 mg/kg once a day for 16 weeks after the establishment of DCM model), and control group (n = 8, fed with normal diet and perfused into the stomach with normal saline once daily for 16 weeks). At the end of the experiment, the contents of fast blood-glucose (FBG), fast insulin (FIN), serum cholesterol, and triglyceride were detected, and insulin sensitivity index (ISI) was calculated. Cardiac catheterization was performed to measure the hemodynamics indexes: left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), and maximal rise/fall velocity of ventricular pressure (+/- dp/dt(max)), and the left ventricular diastolic function (T) was calculated. Pieces of myocardium tissue were taken out to undergo ultrastructural histopathological examination by transmission electron microscopy. The content of collagen was quantified by Masson three-color staining. Real-time RT-PCR and Western-blotting were used to detect the mRNA expression and protein expression of TGFbeta(1), TGFbetaRII, Smad2, Smad3, and Smad7. By the end of experiment the levels of FBG, triglyceride, and cholesterol increased and the ISI decreased significantly in the DCM and valsartan groups (all P < 0.01). Compared with the valsartan and control groups the levels of LVEDP and T significantly increased, and the levels of LVSP and +/- dp/dt(max), significantly decreased (all P < 0.01); and the LVEDP of the valsartan group was significantly higher than that of the control group and the +/- dp/dt(max) of the valsartan group was significantly lower than that of the control group (P < 0.01). The volume of collagen in the myocardial tissue of the DCM group was 17% +/- 3%, significantly higher than that of the control group (11% +/- 3%, P < 0.01). The content of collagen in the myocardial tissue of the valsartan group was lower significantly than that of the DCM group. The levels of mRNA expression of TGFbeta(1), TGFbetaRII, Smad2, and Smad3 were 0.0126 +/- 0.0057, 0.0877 +/- 0.0272, 0.0884 +/- 0.0146, and 0.012 +/- 0.0048 respectively, all significantly higher than those of the control group (0.0054 +/- 0.0009, 0.0523 +/- 0.0218, 0.0413 +/- 0.0186, and 0.0064 +/- 0.0021 respectively, all P < 0.05 - 0.01). The ratios Smad2/Smad7 and Smad3/Smad7 of the DCM group were significantly higher than those of the control group (both P < 0.05). The protein levels of TGFbeta(1), P-Smad2, and P-Smad3 were 143 +/- 17, 212 +/- 43, and 151 +/- 32 respectively, all significantly higher than those of the control group (103 +/- 18, 107 +/- 21, and 89 +/- 17 respectively, P < 0.01). The P-Smad2/Smad7 and P-Smad3/Smad7 of the DCM group were significantly higher than those of the control group (both P < 0.05), The Smad2/Smad7 (or P-Smad2/Smads7) and Smad3/Smad7 (or P-Smad3/Smads7) of the valsartan group was significantly lower than those of the DCM group (both P < 0.05). Activation of TGFbeta(1)/Smads signal pathway and imbalance between Smad2, 3 and Sma7 may be one of the mechanisms of myocardial interstitial fibrosis in DCM. Valsartan can prevent myocardium from damage by blocking the signal pathway.
    Zhonghua yi xue za zhi 02/2007; 87(6):366-70.
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    ABSTRACT: Hyperglycemia could upregulate transforming growth factor-beta (TGFbeta(1)) via thrombospondin (TSP-1) and induce fibrotic renal disease in the rat in vivo and myocardial fibrosis was related to cardiac dysfunction in diabetic patients. We explored the role of glucose/TSP-1/TGFbeta(1) signal pathways in the development of diabetic cardiomyopathy (DCM). Male Wistar rats were fed with high cholesterol diet for 17 weeks, streptozocin (30 mg/kg, i.p) was given at the 28th day, rats with fasting blood glucose > or = 11.1 mmol/L by the end of the 5th week were assigned to DCM group (n = 11). Control rats (n = 8) were fed with regular chow. Fasting blood glucose (FBG) was monitored throughout the study. After hemodynamic measurements by the end of the study, myocardial collagen content was quantified in Masson-stained samples and the mRNA expressions of TSP-1 and TGFbeta(1) were detected by quantification real-time RT-PCR. The protein levels of TSP-1, active and latent TGFbeta(1) were detected by Western blot. Compared with control group, cardiac function was decreased as shown by significantly reduced left ventricular systolic pressure, dp/dt(max) and dp/dt(min), while the myocardial collagen content was significantly increased in the DCM group (11.01 +/- 3.05 vs. 16.92 +/- 3.18, P < 0.01). The myocardial mRNA expressions of TSP-1, TGFbeta(1) and protein expressions of TSP-1, active and latent TGFbeta(1) in the DCM group were also significantly higher than those of the control group. Moreover, myocardial collagen was positively correlated to FBG (r = 0.746, P < 0.01); mRNA expressions of TSP-1 and TGFbeta(1), protein expressions of TSP-1 and active TGFbeta(1) were positively correlated to FBG and myocardial collagen (P < 0.05). However, there were no correlations between the protein expression of latent TGFbeta(1) and FBG and myocardial collagen. The pathway of glucose/TSP-1/TGFbeta(1) might play an important role in myocardial interstitial fibrosis of DCM. It may be the basis of novel therapeutic approaches for ameliorating DCM.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 03/2006; 34(3):217-21.
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    ABSTRACT: Tribbles, a protein family controlling mitogen-activated protein kinase cascades, might contribute to the remodeling process in dilated cardiomyopathy. We investigated the gene expression of Tribble 3 (TRB(3)), cardiac function and collagen changes in rats with diabetic cardiomyopathy (DCM) and the modulating effects of valsartan on them. Male Wistar rats were fed with high cholesterol diet throughout the study period, streptozocin (30 mg/kg, i.p) was given at the 28th day, valsartan (30 mg.kg(-1).d(-1), n = 13) or placebo (n = 11) was administered at the 35th day to rats with fasting blood glucose > or = 11.1 mmol/L per gavage for another 12 weeks. Control rats (n = 8) were fed with regular chow. Fasting blood glucose was monitored throughout the study, left ventricular function was determined by echocardiography, myocardial collagen content quantified after Masson-staining and myocardial mRNA expression of TRB(3) detected by quantification real-time RT-PCR at the end of study. Cardiac function was significantly improved (EF: 74% +/- 10% vs. 66% +/- 7%, P < 0.05), myocardial collagen content decreased (13.23 +/- 3.14 vs. 16.92 +/- 3.18, P < 0.05) in rats with DCM treated with valsartan. Moreover, TRB(3) mRNA was significantly increased in rats with DCM compared to control rats (0.0198 +/- 0.0082 vs. 0.1108 +/- 0.0933, P < 0.05) and the increase could be significantly attenuated by valsartan (0.0367 +/- 0.0234, P < 0.05 vs. DCM). A significant positive correlation was observed between myocardial TRB(3) mRNA and myocardial collagen content (r = 0.67, P < 0.05) and between TRB(3) mRNA and fasting blood glucose (r = 0.69, P < 0.05) in rats with DCM. Our results show for the first time that myocardial TRB(3) mRNA is upregulated in rats with DCM and which could be down-regulated by valsartan.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 03/2006; 34(3):212-6.
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    ABSTRACT: To investigate the mechanism of reversion of myocardial interstitial fibrosis in diabetic cardiomyopathy (DCM) by valsartan. Forty male wistar rats were randomly divided into 3 groups: DCM group, n = 16, fed with high-fat diet for 4 weeks and injected intraperitoneally with streptozocin (STZ) once to induce hyperglycemia so as to construct a DCM model, and then perfused into the stomach with normal saline; valsartan group, n = 16, to be constructed into DCM model and then perfused into the stomach with valsartan once daily; and control group (n = 8, fed with normal food and perfused into the stomach with normal saline. Four weeks after feeding (i.e., before injection of STZ), 1 week after STZ injection, and by the end of experiment after 12-hour fasting samples of venous blood were collected to detect the contents of triglyceride and fasting blood-glucose and insulin; by the end of experiment miniature cardiac catheter was inserted into the left ventricle to conduct hemodynamic examination. Then myocardium tissues were collected, collagen content was detected by Masson staining, real-time RT-PCR was used to detect the mRNA expression of thrombospondin (TSP)-1 and tumor growth factor (TGF)-beta(1) mRNA, expression, and Western blotting was used to detect the protein expression of TSP-1, active TGF-beta(1) (A-TGF-beta(1)) and latent TGF-beta(1) (L-TGF-beta(1)). By the end of the experiment, the body weights, and insulin sensitivity index were significantly lower and fasting blood-glucose, and serum triglyceride and cholesterol were significantly higher in the DCM group and valsartan group in comparison with those in the control group (all P < 0.01), however, there was no significant differences in fasting insulin among these 3 groups. The values of left ventricular systolic pressure (LVSP) and +/- dp/dt(max) were significantly lower and left ventricular end diastolic pressure were significantly higher in the DCM group in comparison with the control group (all P < 0.01). The LVSP and -dp/dt(max) were significantly higher and LVEDP was significantly lower in the valsartan group than in the DCM group (all P < 0.05). The LVEDP was significantly higher and -dp/dt(max) was significantly lower in the valsartan group than in the control group. Electron microscopy showed the distribution of a great amount of collagen in the myocardial interstitial tissue. The collagen content of the DCM group was 17 +/- 3, significantly higher than that of the control group (11 +/- 3, P < 0.05), and the collagen content of the valsartan group was 13 +/- 3, significantly lower than that of the DCM group (P < 0.05). The mRNA expression of TSP-1 and that of TGF-beta(1) were significant higher in the DCM group than in the control group (both P < 0.05), and were significantly lower in the valsartan group than in the DCM group (both P < 0.05); however, the TGF-beta(1) mRNA expression in the valsartan group was significantly higher in the valsartan group than in the control group (P < 0.05). The values of protein expression of TSP-1, A-TGF-beta(1) and L-TGF-beta(1) were all significantly higher in the DCM group than in the control group (all P < 0.05), and the values of protein expression of TSP-1 and A-TGF-beta(1) in the valsartan group were both significantly lower than those in the DCM group (both P < 0.05), however, there was no significant difference in the protein expression of L-TGF-beta(1) between the valsartan group and DCM group. Valsartan amelioorates myocardial interstitial fibrosis in DCM via TSP-1/TGF-beta(1) signaling pathway.
    Zhonghua yi xue za zhi 01/2006; 86(4):232-6.