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Objective To investigate the effect and mechanism of salvianolic acid B(SalB)on myocardial fibrosis in diabetic rats based on RhoA/ROCK1 signaling pathway.Methods Diabetic rat model was established by injecting streptozotocin into tail vein of healthy male SD rats.At the end of the 12th week, the collagen fiber expression in the left ventricular myocardium of rats was detected by Sirius Red reagent staining.The protein expressions of α-SMA, Collagen and Collagen III in left ventricular myocardium were detected by Western blot.Cardiac fibroblasts(CFs)were cultured in SD rats by differential adhesion, and CFs were pretreated with different concentrations of SalB(12.5, 25, 50 μmol·L-1)for 1 h, and the optimal dose was determined by high glucose induction.RhoA protein expression in CFs was detected by immunofluorescence; the protein expressions of α-SMA, Collagen , Collagen III, RhoA and ROCK1 in CFs were detected by Western blot.Results Compared with the normal control group, the expression of collagen in left ventricular myocardium of diabetic rats increased significantly, and the expression of α-SMA, Collagen and Collagen III increased significantly.After SalB intervention, the expression of collagen decreased significantly, and the expression of the above proteins decreased significantly(P<0.01).The expression of α-SMA, Collagen , Collagen III, RhoA and ROCK1 in CFs stimulated with 25 mmol·L-1 high glucose for 24 h was significantly increased.After pretreatment with SalB(25 μmol·L-1)and inhibitor Y-27632(10 μmol·L-1), the activity of CFs was significantly inhibited, and the expression of these proteins was significantly decreased(P<0.01).Conclusion SalB can improve myocardial fibrosis in diabetic rats, and has a certain role in protecting the myocardium of diabetic rats.The mechanism may be related to the inhibition of RhoA/ROCK1 signaling pathway.
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Objective: To explore therapeutic effect of pitavastatin on young and middle-aged patients with hyperlipidemia complicated carotid plaques and its influence on vascular endothelial function. Methods: A total of 126 young and middle-aged patients with hyperlipidemia complicated carotid plaques [carotid intima-media thickness (IMT) ＞ 1. 5mm]were selected, and were randomly divided into no lipid lowering treatment group (n=62) and pitavastatin group (n=64). Flow-mediated dilation of brachial artery (FMD), carotid IMT and blood lipid levels before and 12 months after medication, and incidence rate of adverse events were recorded and compared between two groups. Results: Compare with before treatment and no lipid lowering treatment group after treatment, there was significant rise in FMD [(6. 70±2. 10) ％, (6. 60±2. 35) ％ vs. (8. 90±3. 60) ％], and significant reductions in levels of total cholesterol [(6. 05±1. 40) mmol/L, (5. 67±1. 90) mmol/L vs. (4. 05±1. 20) mmol/L], triglyceride [(2. 18± 0. 72) mmol/L, (2. 08±0. 68) mmol/L vs. (1. 77±0. 65) mmol/L]and low density lipoprotein cholesterol [(4. 65±1. 50) mmol/L, (4. 41±1. 36) mmol/L vs. (2. 01±1. 30) mmol/L]in pitavastatin group, P＜0. 05 or＜0. 01; there were no significant changes in IMT in two groups. No obvious adverse reaction was found in pitavastatin group. Conclusion: Pitavastatin can significantly improve lipid levels and vascular endothelial function in young and middle-aged patients with hyperlipidemia complicated carotid plaques.
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<p><b>AIM</b>To study the effect of diabetes-like environment on the cardiac hypertrophy, cultured cardiomyocytes were used to study the effect of high insulin and high glucose on norepinephrine (NE)-induced cardiac hypertrophy.</p><p><b>METHODS</b>Using cultured myocardial cells as a model, the cellular hypertrophy was observed. The contracting frequency was counted by the inverted microscope, the protein content was assayed with Lowry's method, the cardiomyocytes' volumes were measured by computer photograph analysis system, the protein synthesis was assayed with [3H] leucine intake method.</p><p><b>RESULTS</b>The total cellular protein content, cellular volumes, cellular protein synthesis showed an increase in high insulin group and high glucose group compared with control group. High insulin and high glucose and NE group showed a further increase compared with high glucose and NE group.</p><p><b>CONCLUSION</b>The high insulin itself induces hypertrophy of the cultured myocardial cells slightly. Meanwhile, imitating diabetes-like environment with high insulin and high glucose and NE can further accelerate hypertrophy of the cultured myocardial cells.</p>