27 results on '"He Jian-Gui"'
Search Results
2. Comparative outcomes of heart failure among existent classes of anti-diabetic agents: a network meta-analysis of 171,253 participants from 91 randomized controlled trials
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Yang, Da-ya, He, Xin, Liang, Hui-wei, Zhang, Shao-zhao, Zhong, Xiang-bin, Luo, Chu-fan, Du, Zhi-min, He, Jian-gui, Zhuang, Xiao-dong, and Liao, Xin-xue
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- 2019
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3. Comparative cardiovascular outcomes in the era of novel anti-diabetic agents: a comprehensive network meta-analysis of 166,371 participants from 170 randomized controlled trials
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Zhuang, Xiao-dong, He, Xin, Yang, Da-ya, Guo, Yue, He, Jian-gui, Xiao, Hai-peng, and Liao, Xin-xue
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- 2018
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4. The nonpeptide AVE0991 attenuates myocardial hypertrophy as induced by angiotensin II through downregulation of transforming growth factor-β1/Smad2 expression
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He, Jian-Gui, Chen, Sheng-Long, Huang, Yi-Yi, Chen, Yi-Li, Dong, Yu-Gang, and Ma, Hong
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- 2010
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5. Acute myocardial ischemia directly modulates the expression of brain natriuretic peptide at the transcriptional and translational levels via inflammatory cytokines
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Xia, Wen-Jing, Huang, Yi-Yi, Chen, Yi-Li, Chen, Sheng-Long, and He, Jian-Gui
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- 2011
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6. B-type natriuretic peptide attenuates cardiac hypertrophy via the transforming growth factor-β1/smad7 pathway in vivo and in vitro
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He, Jian-Gui, Chen, Yi-Li, Chen, Bai-Li, Huang, Yi-Yi, Yao, Feng-Juan, Chen, Sheng-Long, and Dong, Yu-Gang
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- 2010
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7. EPIGALLOCATECHIN-3-GALLATE ATTENUATES CARDIAC HYPERTROPHY IN HYPERTENSIVE RATS IN PART BY MODULATION OF MITOGEN-ACTIVATED PROTEIN KINASE SIGNALS
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Chen, Dan-Dan, Dong, Yu-Gang, Liu, Dan, and He, Jian-Gui
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- 2009
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8. More favorable response to cardiac resynchronization therapy in women than in men.
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Cheng, Yun-Jiu, Zhang, Jing, Li, Wei-Jie, Lin, Xiao-Xiong, Zeng, Wu-Tao, Tang, Kai, Tang, An-Li, He, Jian-Gui, Xu, Qing, Mei, Mei-Yi, Zheng, Dong-Dan, Dong, Yu-Gang, Ma, Hong, and Wu, Su-Hua
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- 2014
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9. GW25-e5170 Estrogen inhibits cardiac hypertrophy via upregulation of B-type natriuretic peptide expression in primary neonatal cardiomyocytes
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Wu, Ling-Ling, Chen, Yi-Li, Huang, Yi-Yi, He, Xin, Zhou, Yue, and He, Jian-Gui
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- 2014
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10. Illness perception among Chinese patients with acute myocardial infarction
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Yan, Jun, You, Li-Ming, He, Jian-Gui, Wang, Jing-Feng, Chen, Lin, Liu, Bai-Ling, Zhou, Jing-Jing, Chen, Jing-Hua, and Jin, Shang-Yi
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MYOCARDIAL infarction , *PSYCHOLOGY of the sick , *CHINESE people , *DISEASE risk factors , *AFFECT (Psychology) , *PREDICTION models , *PSYCHOLOGY of hospital patients , *RESEARCH methodology , *PATIENTS - Abstract
Objective: To explore illness perception (IP) and its predictors among Chinese patients with myocardial infarction (MI). Methods: The revised Illness Perception Questionnaire (IPQ-R) was used in the present study. A cross-sectional, descriptive design was employed. The study was conducted in four major hospitals in Guangzhou (China) with a sample of 193 MI patients. Pearson''s and Spearman''s correlation, t test, one-way ANOVA, factor analysis and multiple linear regression were used. Results: Among the 12 common symptoms of MI, on average only 3.37 were recognized by the subjects. Among the six factors of the cause dimension, “immune factors” received the highest score, followed by “gene and chance”, “behavioral factors”, “psychological factors”, “environmental factors”, and “physical factors”. Subjects perceived MI as a chronic, cyclic illness with serious consequences that could be controlled through treatment, and believed that they had a negative affective response to MI. Furthermore, the dimensions of patients’ IP were correlated, and illness-related factors and socio-demographic factors acted as predictors of IP. Conclusion: The IP of Chinese patients with MI needs to be improved. Practice implications: Based on our findings, effective interventions can be designed to promote MI patients’ IP to facilitate their coping strategies after an episode of MI. [Copyright &y& Elsevier]
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- 2011
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11. Chronic angiotensin-(1–7) administration improves vascular remodeling after angioplasty through the regulation of the TGF-β/Smad signaling pathway in rabbits
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Zeng, Wutao, Chen, Weiyan, Leng, Xiuyu, He, Jian gui, and Ma, Hong
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ANGIOTENSINS , *TISSUE remodeling , *ANGIOPLASTY , *MYOCARDIAL infarction , *TRANSFORMING growth factors , *CELLULAR signal transduction , *LABORATORY rabbits , *RENIN-angiotensin system , *GENE expression - Abstract
Abstract: Objective: Angiotensin-(1–7) [ANG-(1–7)] has been reported to attenuate neointimal formation after vascular injury and stent implantation in rats, but the mechanism remains mostly unresolved. Interestingly, the levels of circulating transforming growth factor-beta1 (TGF-β1) after myocardial infarction were suppressed by ANG-(1–7), which suggests a possible downstream target for the anti-remodeling action of ANG-(1–7). Our study focused on the effects of ANG-(1–7) on vascular remodeling, including neointimal formation and collagen synthesis, and determining whether or not these effects were dependent upon the TGF-β signaling pathway. Methods: Thirty-two New Zealand white rabbits underwent sham surgery or angioplasty in abdominal aorta. The animals were divided into four groups, which were sham, control, ANG-(1–7), and ANG-(1–7)+A-779. Subsequently, an osmotic minipump was implanted to deliver saline, ANG-(1–7) (576μgkg−1 d−1) or ANG-(1–7)+A-779 (576μgkg−1 d−1) for 4weeks. Results: The ANG-(1–7) group displayed a significant reduction in neointimal thickness (207.51±16.70μm vs. 448.08±15.30μm, P <0.001), neointimal area (0.266±0.009mm2 vs. 0.408±0.002mm2, P <0.001), and restenosis rate (28.13±2.74% vs. 40.13±2.74%, P <0.001) when compared to the control group. ANG-(1–7) also inhibited collagen synthesis by significantly decreasing the mRNA expression of Collagen I and Collagen III (vs. Control group: 0.2190±0.0036 vs. 0.3852±0.0212, P <0.001 and 1.1328±0.0554 vs. 1.7378±0.1164, P <0.001, respectively). Furthermore, the expression of TGF-β1 and phosphor-Smad2 (p-Smad2) were significantly suppressed by ANG-(1–7) (vs. Control group: 1.21±0.07 vs. 1.54±0.08, P <0.001 and 0.31±0.01 vs. 0.43±0.02, P <0.001, respectively), but no effect on p38 phosphorylation was observed. [d-Ala7]-ANG-(1–7) (A-779), showed a tendency to attenuate the anti-remodeling effects of ANG-(1–7). Conclusion: ANG-(1–7) decreases the amount of vascular remodeling, including a reduction in neointimal formation and collagen synthesis, after angioplasty in rabbits. The responsible mechanism may function through the possible down-regulation of TGF-β1 levels and inhibition of the Smad2 pathway. [Copyright &y& Elsevier]
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- 2009
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12. Reply.
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Wu, Su-Hua, Lin, Xiao-Xiong, Cheng, Yun-Jiu, Dong, Yu-Gang, Tang, An-li, He, Jian-Gui, Liu, Jun, and Ma, Hong
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- 2013
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13. [Angiotensin-(1-7) reduced postangioplasty vascular fibrosis in abdominal aorta of rabbits].
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Zeng WT, Chen WY, Leng XY, He JG, and Ma H
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- Animals, Aorta, Abdominal metabolism, Aorta, Abdominal pathology, Collagen Type I metabolism, Collagen Type III metabolism, Rabbits, Signal Transduction, Smad2 Protein metabolism, Transforming Growth Factor beta1 metabolism, Angiotensin I pharmacology, Aorta, Abdominal drug effects, Fibrosis metabolism, Muscle, Smooth, Vascular metabolism, Peptide Fragments pharmacology
- Abstract
Objective: To explore the effects of Angiotensin (ANG)-(1-7) on postangioplasty fibrotic remodeling and the involvement of TGF-beta/Smad signaling pathway in this process., Methods: Thirty two healthy New Zealand white rabbits were randomly divided into 4 groups: sham group, control group, ANG-(1-7) group and ANG-(1-7) + A-779 group. Rabbits underwent angioplasty in the abdominal aorta or sham surgery. Subsequently, an osmotic minipump was implanted for saline, ANG-(1-7) (576 microg x kg(-1) x d(-1)) or ANG-(1-7) + A-779 (576 microg x kg(-1) x d(-1)) delivery. Before and after 4 weeks treatment, the levels of ANG II in plasma were measured by ELISA. At week 4, angiography and histomorphometric analysis were performed, mRNA levels of collagen I and III were assayed by RT-PCR and protein levels of TGF-beta1 and Smad2 in local vessel were assayed by Western blot., Results: Following 4 weeks treatment, ANG-(1-7) and ANG-(1-7) + A-779 group displayed a significant elevation in lumen diameter [(4.11 +/- 0.10) mm and (3.34 +/- 0.11) mm vs. (2.88 +/- 0.08) mm, P < 0.05, respectively] and reduction in neointimal thickness [(208 +/- 17) microm and (407 +/- 25) microm vs. (448 +/- 15) microm, P < 0.05, respectively], neointimal area [(0.27 +/- 0.09) mm2 and (0.38 +/- 0.01) mm2 vs. (0.41 +/- 0.02) mm2, P < 0.05, respectively] and restenosis rate [(28.1 +/- 2.7)% and (36.8 +/- 2.2)% vs. (40.1 +/- 2.7)%, P < 0.05, respectively] compared with control group. Collagen I, III mRNA and TGF-beta1, Smad2 protein levels were significantly elevated in control group, ANG-(1-7) group and ANG-(1-7) +A-779 group compared to sham group (P < 0.01 or P < 0.05) and reduced in ANG-(1-7) group compared to control group (all P < 0.05). Co-treatment with A-779 reversed the inhibitory action of ANG-(1-7). Plasma levels of ANG II postangioplasty were similar in control and ANG-(1-7) group and both were significantly higher than preoperation levels., Conclusion: ANG-(1-7) attenuates postangioplasty collagen synthesis in rabbits possibly through down-regulating the expression of TGF-beta1 and inhibiting the activation of Smad2 pathway.
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- 2010
14. B-type natriuretic peptide attenuates cardiac hypertrophy via the transforming growth factor-ß1/smad7 pathway in vivo and in vitro.
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He JG, Chen YL, Chen BL, Huang YY, Yao FJ, Chen SL, and Dong YG
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- Animals, Cardiomegaly pathology, Cells, Cultured, Dose-Response Relationship, Drug, Male, Natriuretic Peptide, Brain administration & dosage, Rats, Rats, Sprague-Dawley, Signal Transduction drug effects, Cardiomegaly metabolism, Cardiomegaly prevention & control, Natriuretic Peptide, Brain therapeutic use, Signal Transduction physiology, Smad7 Protein physiology, Transforming Growth Factor beta1 physiology
- Abstract
1. Previously, we showed that long-term treatment of rats after myocardial infarction (MI) with B-type natriuretic peptide (BNP) prevented ventricular remodelling. However, it is unclear whether long-term BNP treatment affects cardiac hypertrophy and, if so, its mechanism of action. In the present study, we investigated the effects of long-term BNP treatment on cardiac hypertrophy and the molecular mechanisms involved. 2. Cardiac hypertrophy was established in rats by ligation of the left anterior descending coronary artery. After treatment with BNP (5 or 15 microg/kg per day) for 8 weeks, indices of cardiac hypertrophy were determined. In separate in vitro experiments, cardiomyocyte hypertrophy was induced by treatment of cardiomyocytes with 10(-6) mol/L angiotensin (Ang) II for 48 h and cell surface area and [(3)H] incorporation were measured. Transforming growth factor (TGF)-beta1 and smad7 mRNA and protein expression in vivo and in vitro were detected using reverse transcription-polymerase chain reaction and western blotting. 3. Long-term BNP treatment dose-dependently attenuated cardiac hypertrophy and improved cardiac function in rats after MI. Furthermore, BNP attenuated the upregulation of TGF-beta1 and downregulation of smad7 mRNA and protein expression. The in vitro experiments further proved that BNP inhibited cardiac hypertrophy and changes in the TGF-beta1/smad7 pathway, which were completely blocked by the cyclic GMP-dependent protein kinase (PKG) inhibitor, KT5823 (cells were treated with 10(-6) mol/L KT5823 for 48 h). 4. The results of the present study demonstrate that long-term treatment of rats with BNP dose-dependently attenuates cardiac hypertrophy and that this is associated with downregulation of TGF-beta1 and upregulation of smad7 via PKG signalling. Long-term BNP treatment may be a new therapeutic strategy to prevent cardiac hypertrophy and progression to heart failure.
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- 2010
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15. [Side effects of non-steroidal anti-inflammatory drugs on gastric mucosa and preventive effects of teprenone].
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Ma SY, Xiong LS, Dong YG, Yang XY, Gao XR, He JG, Liang LQ, Cui Y, and Chen MH
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- Adult, Aged, Cyclooxygenase 1 metabolism, Cyclooxygenase 2 metabolism, Female, Follow-Up Studies, Gastric Mucosa metabolism, Humans, Male, Middle Aged, Prospective Studies, Young Adult, Anti-Inflammatory Agents, Non-Steroidal adverse effects, Diterpenes pharmacology, Gastric Mucosa drug effects
- Abstract
Objective: To evaluate the side effects of non-steroidal anti-inflammatory drugs (NSAID) on gastric mucosa, and to study the preventive effects of teprenone in patients., Methods: 108 patients taking NSAID for more than 3 months with no infection of helicobacter pylori (Hp) were collected. All patients were screened by endoscopy and their upper gastrointestinal symptoms were evaluated. Then, 16 patients with ulcers were excluded and 92 patients were randomly divided into intervention group with teprenone and control group. After follow-up for 3 months, patients were screened again by endoscopy and their upper gastrointestinal symptoms were also evaluated. Specimens of gastric mucosa were studied by PAS dyeing, and Cyclooxygenase (COX) level were evaluated by immunohistochemical technique., Results: Of patients taking NSAIDs, the erosion was found in 48 (44.4%) patients while 16 (14.8%) were found with peptic ulcers. The damages were improved significantly (Z = -4.96, P = 0.000) in the intervention group with teprenone (n = 45) as compared with control group (n = 47) after follow-up for 3 months. Both the cox-1 level [31.1% (14/45) vs 6.7% (3/45), P = 0.003] and mucus thickness [66.7% (30/45) vs 13.3% (6/45), P= 0.000] also increased in the intervention group as compared with control group. No significant difference was found on COX-2 level between these two groups [28.9% (13/45) vs 31.1% (14/45), P = 0.82]., Conclusion: Long-term use of NSAID caused severe damages on gastric and duodenal mucosa; teprenone improved NSAID-related gastric side effects and increased the COX-1 level and mucus thickness.
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- 2009
16. [Effects of rhBNP on left ventricular remodeling in rats with acute myocardial infarction].
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FAN YQ, HE JG, CHEN YL, Chen G, MA H, ZHOU XL, HU XW, PENG HW, and ZHAO B
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- Animals, Disease Models, Animal, Male, Myocardial Infarction physiopathology, Rats, Rats, Sprague-Dawley, Recombinant Proteins therapeutic use, Myocardial Infarction drug therapy, Natriuretic Peptide, Brain therapeutic use, Ventricular Remodeling drug effects
- Abstract
Objective: To assess the effects of rhBNP on left ventricular (LV) remodeling in rats with acute myocardial infarction (AMI)., Methods: AMI was induced by ligating coronary artery in male Sprague Dawley rats. Two days after surgery, AMI rats received intravenous infusion of rhBNP (15 microg/kg or 5 microg/kg once daily, n = 15 each) or saline (placebo control, n = 15) through Jugular Vein. Sham-operated rats (n = 15) served as normal control. Four weeks later, hemodynamic measurements were performed, left ventricular weight (LVW), ratio of left ventricular weight to body weight (LVW/BW), left ventricular diameter (LVD) and infarct size were determined. Plasma angiotensin II and myocardial angiotensin II levels were also measured., Results: Compared with sham-operated rats, LVW, LVW/BW, LVD and myocardial angiotensin II level were significantly increased, while the LV systolic pressure (LVSP), +/- dp/dt were significantly reduced in saline treated AMI rats (all P < 0.05). LVW/BW, MI size, LVD and myocardial angiotensin II in rhBNP treated AMI rats were significantly lower [LVW: (492.6 +/- 34.0) mg, (498.8 +/- 47.8) mg, (570.0 +/- 24.2) mg, P < 0.01; LVW/BW: 2.0 +/- 0.2, 2.0 +/- 0.2, 2.3 +/- 0.1, P < 0.01; LVD: (25.3 +/- 2.9)%, (31.4 +/- 3.0)%, (46.4 +/- 3.0)%, P < 0.01; myocardial angiotensin II: (881.3 +/- 62.7) pg/L, (1186.0 +/- 94.5) pg/L, (2436.7 +/- 280.3) pg/L, P < 0.05], while LVSP and +/- dp/dt in rhBNP treatment groups were significantly increased than saline treated AMI rats (P < 0.05 or P < 0.01)., Conclusion: RhBNP is effective in attenuating left ventricular remodeling after AMI in rats.
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- 2008
17. [Effect of chronic enhanced external counterpulastion on gene expression profiles of arterial endothelial cells of pigs fed with high-cholesterol diet].
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He XH, Wu GF, Zhang Y, Chen XL, Zhang ZS, Zhan CY, Liu J, He JG, Xiong Y, Fang DQ, Liang LG, Qian YT, Lin GF, Dai G, Feng MZ, Wang KJ, Zhu ZY, and Ma H
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- Animals, Aorta, Abdominal metabolism, Aorta, Abdominal pathology, Arteriosclerosis etiology, Arteriosclerosis pathology, Coronary Vessels metabolism, Coronary Vessels pathology, Diet, Atherogenic, Male, Oligonucleotide Array Sequence Analysis methods, Swine, Arteriosclerosis genetics, Counterpulsation methods, Endothelial Cells metabolism, Gene Expression Profiling
- Abstract
Objective: To investigate the effect of chronic enhanced external counterpulastion (EECP) on gene expression profiles of arterial endothelial cells (ECs) of pigs fed with high-cholesterol diet., Methods: Eight male pigs were fed with high-cholesterol diet for 12 weeks to induce arteriosclerosis and subjected to EECP for accumulative 36 h (2 h every other day for 18 sessions). Another 8 pigs on cholesterol-enriched diet and 6 normally fed pigs served as the arteriosclerosis model group and normal control group, respectively, and the high-cholesterol diet was maintained until the end of EECP treatment. The coronary artery was then isolated for transmission electro microscopy, and the abdominal aorta was observed using Sudan III staining. The gene expression profiles in ECs from the thoracic aorta using cDNA microarrays., Results: Macrophages and foam cells were detected beneath the ECs in the coronary artery of pigs in the model group, but not in the other two groups. The ratios of Sudan III-positive area in the celiac aorta were significantly lower in normal control and EECP groups than in the model control group (P<0.05). Compared with the normal control group, the gene expressions of integrins-beta1 and CTGF were up-regulated in the model group. Compared with the model group, the expressions of integrins-beta1, CTGF and VCAM-1 were down-regulated and eNOS up-regulated in EECP group., Conclusion: Chronic EECP may reduce endothelial injury, down-regulate the gene expression level of integrin-beta1, CTGF and VCAM-1, lower cholesterol uptake and attenuate arterial endothelial inflammation to protect the pigs fed with high-cholesterol diet from arteriosclerosis.
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- 2008
18. [An experimental study of expression of angiotension converting enzyme 2 in myocardium and effect of telmisartan treatment in pressure-overloaded rats].
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Wang LJ, Ma H, Liao XX, He JG, Zhang WW, Tian F, Cai YM, Gu HB, Hao YH, Hu XS, Zou HM, and Zhou QL
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- Angiotensin II metabolism, Angiotensin-Converting Enzyme 2, Animals, Aortic Coarctation drug therapy, Disease Models, Animal, Male, RNA, Messenger metabolism, Random Allocation, Rats, Rats, Sprague-Dawley, Telmisartan, Aortic Coarctation metabolism, Benzimidazoles pharmacology, Benzoates pharmacology, Myocardium metabolism, Peptidyl-Dipeptidase A metabolism
- Abstract
Objective: To study the effect of hypertension and telmisartan treatment on the protein and gene expression of cardiac angiotensin-converting enzyme 2 (ACE2) in pressure-overloaded rats., Methods: Coarctation of suprarenal abdominal aorta was reproduced in 8 week-old male Sprague-Dawley (SD) rats and then randomized into 4 groups, including a sham group (n=15), a suprarenal aortic coarctation group (model group, n=12), a suprarenal aortic coarctation with low-dose Telmisartan treatment group (low-dose group, 2 mgxkg(-1)xd(-1), n=11) and a suprarenal aortic coarctation with high-dose Telmisartan treatment group(high-dose group, 10 mgxkg(-1)xd(-1), n=13). Telmisartan or equivalent amount of normal saline was gavaged 24 hours before the operation and once every day afterwards for 3 weeks. At the end of 3 weeks, the concentrations of angiotensin (AngII) in plasma and myocardium were measured by radioimmunoassay. Changes in both protein quantity and gene expressions of both ACE2 and ACE were determined by Western blotting analysis and reverse transcription-polymerase chain reaction (RT-PCR) technique, respectively., Results: Suprarenal abdominal aortic coarctation induced a significant increase in the plasma and myocardium AngII concentration [plasma: (495.1+/-55.6) ng/L vs. (269.2+/-39.5)ng/L, myocardium: (103.6+/-23.7) ng/g vs. (49.5+/-13.5) ng/g, both P<0.01] and expressions of gene and protein of ACE (P<0.01) and ACE2 (P<0.05). Telmisartan further increased the concentration of AngII in plasma and myocardium in a dose-dependent manner [plasma: (702.2+/-40.6) ng/L vs. (612.6+/-35.5) ng/L, myocardium (211.5+/-21.5) ng/g vs. (189.6+/-43.6) ng/g, both P<0.05], and induced a dose-dependent increase in both protein and gene expression of ACE2 (protein 1.16+/-0.06 vs. 0.79+/-0.04, gene 0.54+/-0.08 vs. 0.41+/-0.04, both P<0.05). Expression of ACE2 protein in low-dose and high-dose groups was increased by 1.0 and 1.58 folds respectively, and gene was increased by 1.3 and 1.6 folds (all P<0.05). The expression of ACE protein and gene in model group increased significantly (protein: 2.10+/-1.07 vs. 1.02+/-0.05, gene: 1.93+/-0.09 vs. 0.26+/-0.09, both P<0.01). Telmisartan had no significant effect on ACE gene and protein expressions (both P>0.05)., Conclusion: Suprarenal abdominal aortic coarctation induced a significant increases of ACE and ACE2 gene and protein expressions. Telmisartan induces a dose-dependent increases of cardiac ACE2 gene and protein expression,which may be the mechanism of its therapeutic effects.
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- 2008
19. [Ischemic postconditioning attenuates ischemia/reperfusion injury in isolated hypertrophied rat heart].
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Peng LY, Ma H, He JG, Gao XR, Zhang Y, He XH, Zhai YS, and Zhang XJ
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- Animals, Glycogen Synthase Kinase 3 metabolism, Glycogen Synthase Kinase 3 beta, Male, Myocardial Reperfusion Injury metabolism, Phosphatidylinositol 3-Kinases metabolism, Proto-Oncogene Proteins c-akt metabolism, Random Allocation, Rats, Rats, Sprague-Dawley, Signal Transduction, Ischemic Preconditioning, Myocardial, Myocardial Reperfusion Injury therapy
- Abstract
Objective: To explore the effects of ischemic postconditioning on ischemia/reperfusion injury in isolated hypertrophied rat heart and investigate the signal transduction pathway changes induced by ischemia postconditioning., Methods: Cardiac hypertrophy was induced in rats by abdominal aortic banding, and isolated hypertrophied rat heart ischemia/reperfusion model was made by Langendorff technique to evaluate the effects of ischemia postconditioning on left ventricular systole pressure, coronary artery flow, creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) release, myocardial infarction size, and the level of myocardial phospho-protein kinase B/Akt (Ser473), phospho-glycogen synthase kinase-3beta (Ser9). Following groups were studied (n = 12 each group): IR, 30 min ischemia (I)/60 min Reperfusion (R); Post: 30 min ischemia, 6 circles of 10 s I/10 s R followed by 60 min R; Post Wort: 30 min ischemia, 6 circles of 10 s I/10 s R, wortmannin (10(-7) mol/L) followed by 60 min R; Wort: 30 min ischemia, wortmannin (10(-7) mol/L) followed by 60 min R., Results: Left ventricular systolic pressure and coronary artery flow were significantly increased, myocardial infarction size and the release of CPK, LDH significantly reduced in Post group compared to that in IR group. Phospho-protein kinase B/Akt (Ser473) and phospho-glycogen synthase kinase-3beta (Ser9) levels were also significantly higher in Post group than that in IR group. Phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin prevented the increase of phospho-protein kinase B/Akt (Ser473) and phospho-glycogen synthase kinase-3beta (Ser9) induced by ischemic postconditioning, but only partly abolished the cardioprotection of ischemic postconditioning., Conclusion: Ischemic postconditioning attenuates ischemia/reperfusion injury in isolated hypertrophied rat heart. The cardioprotective effects of ischemic postconditioning were partly mediated through PI3K/Akt/GSK-3beta signaling pathway.
- Published
- 2006
20. [Study on up-regulation of the expression of angiotensin-converting enzyme-2 in human umbilical vein endothelial cells by telmisartan].
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Wang LJ, Ma H, Liao XX, Hu XS, Tian F, Gu HB, Hao YH, Cai YM, Peng LY, He JG, Zeng WT, and Leng XY
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- Angiotensin-Converting Enzyme 2, Cells, Cultured, Endothelial Cells drug effects, Gene Expression, Humans, Peptidyl-Dipeptidase A genetics, RNA, Messenger genetics, Telmisartan, Umbilical Veins cytology, Up-Regulation, Benzimidazoles pharmacology, Benzoates pharmacology, Endothelial Cells enzymology, Endothelium, Vascular cytology, Peptidyl-Dipeptidase A metabolism
- Abstract
Objective: To investigate the effect of telmisartan on the protein and gene expression of angiotensin-converting enzyme-2 (ACE2) in human umbilical vein endothelial cells (HUVECs)., Methods: HUVECs were treated with various concentrations of telmisartan (10(-7), 10(-6) and 10(-5) mol/L) for 24 hours. In a time-control experiment, HUVECs were treated with telmisartan at the final concentration of 10(-6) mol/L for 6, 12 and 24 hours, respectively. In another experiment, HUVECs were treated with PD123319 (10(-6) mol/L) only or combined with same final concentration of telmisartan for 12 hours, respectively. Changes in both protein and gene expression of ACE2 were determined with Western blot analysis and reverse transcription-polymerase chain reaction (RT-PCR) technique, respectively., Results: Telmisartan induced a concentration and time dependent increase in both protein and gene expression of ACE2 (P<0.05 or P<0.01). Compared with control group, treatment of HUVECs with telmisartan at the concentration of 10(-7), 10(-6) and 10(-5) mol/L stimulated 1.5-, 2.7- and 4.6-fold increase in the ACE2 protein expression, as well as 1.2-, 2.3- and 4.5-fold increase in its gene expression, respectively. After treatment of HUVECs with telmisartan for 6, 12, and 24 hours at the concentration of 10(-6) mol/L, the ACE2 protein expression increased 1.6-, 2.7- and 4.2-fold, and its gene expression increased 1.3-, 2.3- and 4.0-fold, respectively. Compared with control and telmisartan groups, PD123319 had no effect on both protein and gene expression of ACE2 (P>0.05)., Conclusion: Telmisartan up-regulates the protein and gene expression of ACE2 in HUVECs in a concentration and time dependent manner. This effect may be mediated via its specific pathway.
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- 2006
21. [Effects of enhanced external counterpulsation in atherosclerosis and NF-kappaB expression: a pig model with hypercholesterolemia].
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Zhang Y, He XH, Chen XL, Hu RD, Ma H, Wu GF, He JG, Zhan CY, Jin YF, Fang DQ, and Zheng ZS
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- Animals, Aorta, Abdominal metabolism, Aorta, Abdominal pathology, Aorta, Abdominal ultrastructure, Atherosclerosis blood, Atherosclerosis metabolism, Cholesterol blood, Coronary Vessels metabolism, Coronary Vessels pathology, Coronary Vessels ultrastructure, Endothelial Cells metabolism, Endothelial Cells pathology, Hypercholesterolemia blood, Hypercholesterolemia metabolism, Lipoproteins, LDL blood, Male, Microscopy, Confocal, Microscopy, Electron, Scanning, Microscopy, Electron, Transmission, Muscle, Smooth, Vascular metabolism, Muscle, Smooth, Vascular pathology, Random Allocation, Swine, Atherosclerosis pathology, Counterpulsation methods, Hypercholesterolemia pathology, NF-kappa B metabolism
- Abstract
Objective: To study the effects of enhanced external counterpulsation (EECP) on the vascular morphology, and endothelial function using experimentally induced hypercholesterolemic pigs., Methods: Thirty five male pigs were randomly divided into three groups: 7 normal control animals, 11 hypercholesterolemic animals, and 17 hypercholesterolemic animals receiving EECP. Serum cholesterol was measured. The coronary arteries and aortas were sampled for histopathologic and ultrastructural examination. The NF-kappaB protein expression of porcine coronary arteries was investigated by immunofluorescence., Results: Compared with the normal controls, serum cholesterol levels were significantly higher in the hypercholesterolemic animals with or without EECP. The plaque/intimal area ratio of the aorta decreased significantly in animals receiving EECP [(3.33 +/- 2.40)%, versus (12.03 +/- 7.12)% in those without EECP, P < 0.05]. Lipid deposition, endothelial damage and proliferation of smooth muscle cells were less severe in animals receiving EECP than those not. Moreover, activation and expression of NF-kappaB also decreased significantly (P < 0.05) in animals receiving EECP., Conclusions: EECP improves the morphology and function of vascular endothelium, and retards the development and progression of atherosclerosis, likely through the inhibition of NF-kappaB signaling pathway.
- Published
- 2006
22. [Angiotensin-(1-7) modulates fibrinolytic imbalance induced by oxidized low-density lipoprotein in cultured human umbilical vein endothelial cells].
- Author
-
Wang LJ, Ma H, Cai YM, He JG, Liao XX, Zeng WT, Wang LC, and Liu J
- Subjects
- Angiotensin II analogs & derivatives, Angiotensin II pharmacology, Angiotensin Receptor Antagonists, Cells, Cultured, Endothelium, Vascular cytology, Humans, Plasminogen Activator Inhibitor 1 genetics, Tissue Plasminogen Activator genetics, Umbilical Veins cytology, Angiotensin I pharmacology, Endothelium, Vascular metabolism, Lipoproteins, LDL pharmacology, Peptide Fragments pharmacology, Plasminogen Activator Inhibitor 1 biosynthesis, Tissue Plasminogen Activator biosynthesis
- Abstract
Objective: To study the effect of angiotensin-(1-7)[Ang-(1-7)]on fibrinolytic imbalance induced by oxidized low- density lipoprotein (ox-LDL) in cultured human umbilical vein endothelial cells (HUVECs)., Method: Cultured HUVECs were incubated for 24 h in the presence of Ang-(1-7), ox-LDL and A-779 at different concentrations either separately or in combination. The final concentrations of Ang-(1-7) were 10, 100 and 1,000 nmol/L, and those of ox-LDL were 25, 50 and 100 mg protein/L. The final concentration of A-779, an Ang-(1-7) receptor antagonist, was 100 nmol/L. Tissue plasminogen activator (t-PA) and its inhibitor-1(PAI-1) antigen in the medium were determined by enzyme-linked immunosorbent assay (ELISA) and their mRNA levels by reverse transcriptional (RT) PCR., Results: Ox-LDL (25-100 mg protein/L) dose-dependently increased PAI-1 release and up-regulated PAI-1 gene transcription, but decreased t-PA release and down-regulated t-PA gene transcription (P>0.001-0.05). Ang-(1-7) (100-1,000 nmol/L) dose-dependently decreased PAI-1 release and PAI-1 gene transcription (P>0.01-0.05) but had no effect on t-PA release and gene transcription. In the presence of ox-LDL, Ang-(1-7) lowered the increased levels of PAI-1 and PAI-1 mRNA, and elevated the levels of decreased t-PA and t-PA mRNA in the cells (P>0.01-0.05). The effects of Ang-(1-7) could be blocked by A-779., Conclusion: Angiotensin-(1-7) effectively modulates the fibrinolytic imbalance induced by ox-LDL via its specific receptor.
- Published
- 2005
23. [Effects of ACE inhibitor on the calcium transient and calcium handling proteins in ventricular myocytes from rats with heart failure].
- Author
-
Wang LC, Ma H, He JG, Liao XX, Mai WY, Chen WF, Leng XY, Ma L, Zeng WT, Liu J, Tao J, Dong YG, Tang AL, and Feng C
- Subjects
- Animals, Calmodulin metabolism, Heart Failure drug therapy, Male, Myocytes, Cardiac drug effects, Perindopril therapeutic use, Rats, Rats, Wistar, Calcium metabolism, Heart Failure metabolism, Myocytes, Cardiac metabolism, Perindopril pharmacology
- Abstract
Objective: To investigate the influence of ACE inhibitor (perindopril) on the contractility and calcium transient and calcium handling proteins in ventricular myocytes from rats with experimental heart failure., Methods: Male Wistar rats were randomized to heart failure group treated with perindopril (CHF-T, 3 mg.kg(-1).d(-1)), heart failure group without treatment (CHF-C) and sham-operated group (PS) after heart failure was induced by constricting abdominal aorta for 16 weeks. All groups were further followed up for 12 weeks. Left ventricular myocytes were isolated, and single cell shortening fraction and [Ca(2+)](i) were simultaneously measured through laser scanning confocal microscope under the field stimulation (1.0 Hz). RT-PCR and Western blot were performed to evaluate the level of mRNA and protein of Na(+)-Ca(2+) exchanger (NCX(1)), sarcoplasmic Ca(2+)-ATPase (SERCA(2)) and phospholamban (PLB)., Results: The fraction of cell shortening (FS%) and [Ca(2+)](i max) (nmol/L) were significantly smaller in group CHF-C than group PS (FS%: 7.51 +/- 1.15 vs 13.21 +/- 1.49; [Ca(2+)](i max): 330.85 +/- 50.05 vs 498.16 +/- 14.07; both P < 0.01). And in CHF-T group, FS and [Ca(2+)](i max) were greater than those in CHF-C group. In CHF-C group, the left ventricular mRNA of NCX(1) and PLB were significantly higher than those in PS group (R(NCX)(1)/beta-Actin: 0.51 +/- 0.12 vs 0.19 +/- 0.06, P < 0.01; R(PLB)/beta-Actin: 0.26 +/- 0.12 vs 0.20 +/- 0.08, P = 0.045), yet SERCA(2) mRNA was lower than PS group (0.48 +/- 0.10 vs 0.80 +/- 0.11, P < 0.01). In CHF-T group, the mRNA levels of NCX(1) and SERCA(2) were just in the midst of the CHF-C and PS group, and had statistical significance respectively (all P < 0.05). In CHF - C and CHF - T group, the protein levels of NCX(1) were 1.141 +/- 0.047 and 1.074 +/- 0.081 times PS group, respectively (both P < 0.05), and SERCA(2) protein levels were respectively 0.803 +/- 0.100 and 0.893 +/- 0.084 times as high as in PS group (both P < 0.05). The protein expression of NCX(1) and SERCA(2) were also different between CHF-C and CHF-T groups (both P < 0.05)., Conclusion: ACE inhibitor could improve cardiac function in CHF through directly enhancing the contractility of single myocardial cell, and these effects were probably mediated by its role in preventing the deleterious changes of calcium transient and calcium handling proteins in CHF.
- Published
- 2005
24. Effect of angiotensin converting enzyme inhibitor on the calcium transients and calcium handling proteins in ventricular myocytes from rats with heart failure.
- Author
-
Wang LC, Ma H, He JG, Liao XX, Chen WF, Leng XY, Ma L, Mai WY, Tao J, Zeng WT, Liu J, Dong YG, Tang AL, and Feng C
- Subjects
- Animals, Calcium-Binding Proteins genetics, Calcium-Transporting ATPases genetics, Heart Failure metabolism, Heart Ventricles drug effects, Male, Myocytes, Cardiac metabolism, RNA, Messenger analysis, Rats, Rats, Wistar, Sarcoplasmic Reticulum Calcium-Transporting ATPases, Sodium-Calcium Exchanger genetics, Angiotensin-Converting Enzyme Inhibitors pharmacology, Calcium metabolism, Heart Failure drug therapy, Myocytes, Cardiac drug effects, Perindopril pharmacology
- Abstract
Background: Chronic heart failure (CHF) is associated with calcium transients and calcium handling proteins. Angiotensin converting enzyme (ACE) inhibitor has been demonstrated to have beneficial effect on CHF. Yet studies addressed to the relationship between ACE inhibitor and calcium transients in CHF are rare. The aim of this study was to investigate the influence of ACE inhibitor (perindopril) on the contractility and calcium transients and calcium handling proteins in ventricular myocytes from rats with experimental heart failure., Methods: Male Wistar rats were randomized to heart failure group treated with perindopril [CHF-T, 3 mg.kg(-1).d(-1)], heart failure group without treatment (CHF-C) and sham-operated group (PS). Heart failure was induced by abdominal aortic constriction. All groups were further followed up for 12 weeks. Left ventricular myocytes were then isolated. Single cell shortening fraction and [Ca(2+)]i were simultaneously measured by laser scanning confocal microscope under the field stimulation (1.0 Hz). Reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot were performed to evaluate the changes of mRNA and protein of Na(+)-Ca(2+) exchanger (NCX1), sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2) and phospholamban (PLB)., Results: The fraction of cell shortening (FS%) and [Ca(2+)]imax (nmol/L) were significantly reduced in group CHF-C compared with group PS (FS%: 7.51 +/- 1.15 vs 13.21 +/- 1.49; [Ca(2+)]i max: 330.85 +/- 50.05 vs 498.16 +/- 14.07; both P < 0.01), and restored at least partially in CHF-T group. In CHF-C group, the left ventricular mRNA of NCX1 and PLB were significantly upregulated in comparing with PS group (RNCX1/beta-Actin: 0.51 +/- 0.12 vs 0.19 +/- 0.06, P < 0.01; RPLB/beta-Actin: 0.26 +/- 0.12 vs 0.20 +/- 0.08, P < 0.05), while SERCA2 mRNA was downregulated (0.48 +/- 0.10 vs 0.80 +/- 0.11, P < 0.01). The mRNA levels of NCX1 and SERCA2 in CHF-T group were between the CHF-C and PS group, and the differences of the latter two groups were significant (all P < 0.05). In CHF-C and CHF-T groups, the protein expression of NCX1 were 1.141 +/- 0.047 and 1.074 +/- 0.081 times of that in PS group respectively (both P < 0.05), and SERCA2 protein levels were 0.803 +/- 0.100 and 0.893 +/- 0.084 times of that in PS group respectively (both P < 0.05). The protein expression of NCX1 and SERCA2 in the CHF-C and CHF-T groups is significantly different (both P < 0.05)., Conclusion: ACE inhibitor could improve cardiac function of failing heart through directly enhancing the contractility of single cardiomyocyte, and these effects are probably mediated by its roles in preventing the deleterious changes of calcium transients and calcium handling proteins in CHF.
- Published
- 2005
25. Chronic administration of angiotensin-(1-7) attenuates pressure-overload left ventricular hypertrophy and fibrosis in rats.
- Author
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Wang LJ, He JG, Ma H, Cai YM, Liao XX, Zeng WT, Liu J, and Wang LC
- Subjects
- Angiotensin II metabolism, Animals, Antihypertensive Agents administration & dosage, Aortic Coarctation complications, Blood Pressure drug effects, Fibrosis, Male, Myocardium metabolism, Random Allocation, Rats, Rats, Sprague-Dawley, Ventricular Function, Left drug effects, Angiotensin I administration & dosage, Hypertrophy, Left Ventricular drug therapy, Hypertrophy, Left Ventricular pathology, Peptide Fragments administration & dosage
- Abstract
Objective: To test the hypothesis that chronic administration of angiotensin-(1-7) [Ang-(1-7)] attenuates cardiac hypertrophy in rats in vivo., Methods: Coarctation of the suprarenal abdominal aorta was performed in 41 8-week-old male Sprague Dawley rats. Twenty-four hours after the operation, osmotic minipumps were surgically implanted subcutaneously in the rats, which were randomly divided into 3 groups, including a sham-operation group (n=15) receiving infusion with normal saline, a suprarenal aortic coarctation group (n=12), and a suprarenal aortic coarctation group (n=14) with Ang-(1-7) treatment at the dose of 25 mug x kg(-1) x h(-1). Four weeks later, the systolic and diastolic blood pressures were measured and the left ventricular mass index (LVMI, mg/g) was calculated from the ratio of left ventricular weight to body weight. The concentrations of Ang II in the plasma and myocardium were measured by radioimmunoassay, and myocardial interstitial collagen volume fraction (ICVF) was determined by quantitative morphometry of the sections with Picrosirius red staining using an automated image analyzer., Results: Suprarenal abdominal aortic coarctation induced a significant increase in carotid artery systolic and diastolic blood pressure, heart weight, LVMI, ICVF, and the concentration of Ang II in the myocardium (P<0.01). Chronic administration of Ang-(1-7) attenuated the increase in the heart weight, LVMI, ICVF and left ventricular diastolic end pressure (LVEDP) caused by suprarenal abdominal aortic coarctation (P<0.05). Ang-(1-7) also increased the formerly decreased maximum left ventricular pressure reduction rate (-dP/dt(max)) (P<0.05), but had no effect on blood pressure and the concentration of Ang II in the myocardium. No difference was noted in plasma concentration of Ang II between the 3 groups., Conclusions: Ang-(1-7) attenuates cardiac hypertrophy and fibrosis and preserved the impaired left ventricular function induced by left ventricular pressure-overload in rats. These effects are not associated with the changes in the concentrations of Ang II in the left ventricular myocardium and plasma.
- Published
- 2005
26. [Effects of angiotensin-(1-7) on remodeling of myocardial collagen network in pressure-overloaded rats].
- Author
-
He JG, Huang YY, Ma H, He XH, Liao XX, Wang LC, and Zhou JZ
- Subjects
- Animals, Male, RNA, Messenger metabolism, Rats, Rats, Sprague-Dawley, Angiotensins pharmacology, Collagen metabolism, Myocardium metabolism, Ventricular Remodeling drug effects
- Abstract
Objective: To investigate the effects of angiotensin-(1-7) on remodeling of myocardial collagen network in pressure-overloaded rats., Methods: A rat model of pressure-overloaded heart was induced by constriction of abdominal aorta. Seventy-five male Sprague Dawley rats were randomized to sham-operated group, model control group and angiotensin-(1-7) group. The rats of the latter two groups were treated with intravenous infusion of either angiotensin-(1-7) (25 microg x kg(-1) x h(-1)) or saline after operation. Ratio of left ventricular weight to body weight (LVW/BW) and myocardial collagen volume fraction (CVF) were determined at 1 and 4 weeks after operation. And types I and III collagen mRNA expressions were assessed with reverse transcription-polymerase chain reaction (RT-PCR)., Results: At 1 week after the operation, types I and III collagen mRNA expressions of the left ventricular myocardium in model group and angiotensin-(1-7) group were increased significantly compared with those in sham-operated group. But those in angiotensin-(1-7) group were significantly lower than that in model group. At 4 weeks after the operation, LVW/BW and CVF were increased significantly in model group and angiotension-(1-7) group compared with those in sham-operated group, but those in angiotension-(1-7) group were significantly lower than that of model group., Conclusion: Angiotensin -(1-7) can attenuate remodeling of myocardial collagen network in pressure-overloaded rats.
- Published
- 2004
27. Effects of 15-deoxy-delta12,14-prostaglandin J2 on cell proliferation and apoptosis in ECV304 endothelial cells.
- Author
-
Dong YG, Chen DD, He JG, and Guan YY
- Subjects
- Cell Division drug effects, Cells, Cultured, Humans, Mitogen-Activated Protein Kinases metabolism, NF-kappa B metabolism, Prostaglandin D2 analogs & derivatives, Proto-Oncogene Proteins c-myc metabolism, Transcription Factor AP-1 metabolism, Tumor Suppressor Protein p53 metabolism, Umbilical Cord cytology, p38 Mitogen-Activated Protein Kinases, Apoptosis drug effects, Endothelial Cells metabolism, Prostaglandin D2 pharmacology
- Abstract
Aim: To investigate the effects of 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2) on cell proliferation and apoptosis in ECV304 endothelial cells and related molecular mechanism., Methods: MTT, Hoechst33258, TUNEL, Flow cytometry, DNA ladder, RT-PCR, Western blot, and electrophoretic mobility shift assay (EMSA) analysis were employed., Results: The 15d-PGJ2 induced apoptosis in ECV304 endothelial cells in a dose-dependent manner (the percentage of apoptosis was enhanced from 10.0 %+/-1.3 % to 32.8 %+/-1.6 %), which was accompanied by inhibition of NF-?B and AP-1 DNA binding activity, down-regulation of c-myc, upregulation of Gadd45 and p53, and activation of p38 kinase. However, the expression of p21 was found no significant change., Conclusion: peroxisome proliferator-activated receptor gamma ligand, 15d-PGJ2, can inhibit proliferation and induce apoptosis in ECV304 endothelial cells through different mechanisms.
- Published
- 2004
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