Ruofeng Qiu

Poor sleep quality, stress status, and sympathetic nervous system activation in nondipping hypertension.

ObjectiveIt has been reported that poor sleep quality is associated with nondipping hypertension, but the underlying mechanisms were not reported. This study was carried out to evaluate whether poor sleep quality is associated with stress status and sympathetic nervous system activation in nondippers. Materials and methodsA total of 307 Chinese essential hypertensive patients were defined as dippers or nondippers by ambulatory blood pressure monitoring. Sleep quality was assessed by Pittsburgh Sleep Quality Index (PSQI), and stress status was assessed by Perceived Stress Scale (PSS). The levels of epinephrine and norepinephrine were examined to investigate the underlying mechanisms. ResultsA total of 204 (66.4%) and 103 cases (33.6%) were found to be dippers and nondippers, respectively. Nondippers were with poorer sleep quality (P<0.05), more stressful status (P<0.05), and with an increased activity of sympathetic nervous system (P<0.01). The decline of systolic BP (SBP) and diastolic BP (DBP) at night was inversely related with the PSQI score (r=−0.469, P<0.01 and r=−0.421, P<0.01), PSS score (r=−0.432, P<0.01 and r=−0.404, P<0.01), epinephrine (r=−0.304, P<0.05 and r=−0.293, P<0.05), and norepinephrine (r=−0.321, P<0.05 and r=−0.357, P<0.05). Multiple logistic regression analyses showed that older age [odds ratio (OR): 1.69; 95% confidence interval (CI): 1.22–2.43], PSQI score (OR: 2.78; 95% CI: 1.65–6.87), and PSS score (OR: 2.43; 95% CI: 1.56–5.93) were independently correlated with the nondipping pattern. ConclusionPoor sleep quality and stressful status were closely associated with higher activation of sympathetic nervous system, and they are independent predictors of nondipping hypertension.

Lipoprotein-associated phospholipase A2 (Lp-PLA(2)): a novel and promising biomarker for cardiovascular risks assessment.

Atherosclerosis and its manifestations namely cardiovascular diseases (CVD) are still the leading cause of morbidity and mortality worldwide. Although intensified interventions have been applied, the residual cardiovascular (CV) risks are still very high. Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a novel and unique biomarker highly specific for vascular inflammation and atherosclerosis. Both pro-atherogenic property of Lp-PLA2 and positive correlation with CV events have already been demonstrated by a large number of scientific and clinical studies. Currently, in the Adult Treatment Panel III (ATP III) guideline, Lp-PLA2 has been recommended as an adjunct to traditional risk factors in assessing future CV risks. Encouragingly, darapladib, an orally Lp-PLA2 specific inhibitor, has been tested in basic research and preclinical trials and the outcomes are quite striking. Additionally, there are two phase III ongoing clinical trials in evaluating the efficacy and safety of darapladib on cardiovascular outcomes. With regard to the potential values of Lp-PLA2 in risk stratification, therapeutic regimen establishment and prognosis evaluation in patients with moderate or high risk, our present review is going to summarize the relevant data about the bio-chemical characteristics of Lp-PLA2, the actions of Lp-PLA2 on atherosclerosis and the results of Lp-PLA2 in scientific research and clinical studies.

Effects of insulin-like growth factor-1 on the properties of mesenchymal stem cells in vitro.

ObjectiveTo explore the effects of insulin-like growth factor-1 (IGF-1) on migration, proliferation and differentiation of mesenchymal stem cells (MSCs).MethodsMSCs were obtained from Sprague-Dawley rats by a combination of gradient centrifugation and cell culture techniques and treated with IGF-1 at concentrations of 5–20 ng/ml. Proliferation of MSCs was determined as the mean doubling time. Expression of CXC chemokine receptor 4 (CXCR4) and migration property were determined by flow cytometry and transwell migration essay, respectively. mRNA expression of GATA-4 and collagen II was determined by reverse transcription-polymerase chain reaction (RT-PCR).ResultsThe mean doubling time of MSC proliferation was decreased, and the expression of CXCR4 on MSCs and migration of MSCs were increased by IGF-1, all in a dose-dependent manner, while the optimal concentration of IGF-1 on proliferation and migration was different. IGF-1 did not affect the expression of GATA-4 or collagen II mRNA.ConclusionsIGF-1 dose-dependently stimulated the proliferation of MSCs, upregulated the expression of CXCR4, and accelerated migration. There was no apparent differentiation of MSCs to cardiomyocytes or chondrocytes after culturing with IGF-1 alone.

The effect of zolpidem on sleep quality, stress status, and nondipping hypertension

OBJECTIVE Poor sleep quality and stress status have previously been shown to be closely associated with higher activation of the sympathetic nervous system and to be independent predictors of nondipping hypertension. This study aimed to evaluate the effects of the non-hypotensive sedative zolpidem on sleep quality, stress status, and nondipping hypertension. METHODS A total of 103 nondippers were defined as poor or good sleepers by the Pittsburgh Sleep Quality Index. They were randomized to receive zolpidem or placebo treatment for 30 days. Stress status was assessed by the Perceived Stress Scale, and levels of epinephrine and norepinephrine were examined to investigate the underlying mechanisms. RESULTS Poor sleepers treated with zolpidem for 30 days showed significant improvements in sleep quality and stress levels (P<0.01). More nondippers were converted to dippers in the group of poor sleepers treated with zolpidem (11 of 22 patients, 50.0%) than in the placebo (2 of 23, 8.7%) (P<0.01). Epinephrine and norepinephrine levels were significantly reduced in poor sleepers treated with zolpidem (P<0.05). CONCLUSION The results of this study suggest that zolpidem can improve sleep quality and stress status, and can convert nondippers with poor sleep quality into dippers. It may be an option for treating nondipping hypertensive patients with poor sleep quality.

SDF-1α upregulation by atorvastatin in rats with acute myocardial infarction via nitric oxide production confers anti-inflammatory and anti-apoptotic effects

BackgroundThe effects of atorvastatin on SDF-1α expression under acute myocardial infarction (AMI) are still unclear. Therefore, our present study is to investigate the roles and mechanisms of atorvastatin treatment on SDF-1α expression in rats with AMI.MethodsMale Sprague–Dawley rats were underwent permanent coronary artery ligation and randomly assigned into four groups as follow: blank control (B), atorvastatin (A), atorvastatin plus L-NAME (A+L-NAME), and atorvastatin plus AMD3100 (A+AMD3100). Rats underwent similar procedure but without ligation were used as group sham operated (S). Atorvastatin (10mg/Kg/d body weight) was administrated by gavage to rats in three atorvastatin treated groups, and L-NAME (40mg/Kg/d body weight) or AMD3100 (5mg/Kg/d body weight) was given to group A+L-NAME or A+AMD3100, respectively.ResultsComparing with group B, NO production, SDF-1α and CXCR4 expression were significantly up-regulated in three atorvastatin treated groups at the seventh day. However, the increments of SDF-1α and CXCR4 expression in group A+L-NAME were reduced when NO production was inhibited by L-NAME. Anti-inflammatory and anti-apoptotic effects of atorvastatin were offset either by decrease of SDF-1α and CXCR4 expression (by L-NAME) or blockage of SDF-1α coupling with CXCR4 (by AMD3100). Expression of STAT3, a cardioprotective factor mediating SDF-1α/CXCR4 axis induced cardiac protection, was up-regulated most significantly in group A. The effects of atorvastatin therapy on cardiac function were also abrogated either when SDF-1α and CXCR4 expression was diminished or the coupling of SDF-1α with CXCR4 was blocked.ConclusionSDF-1α upregulation by atorvastatin in rats with AMI was, at least partially, via the eNOS/NO dependent pathway, and SDF-1α upregulation and SDF-1α coupling with CXCR4 conferred anti-inflammatory and anti-apoptotic effects under AMI setting which we speculated that ultimately contributed to cardiac function improvement.

Bone marrow stromal cell transplantation combined with angiotensin-converting enzyme inhibitor treatment in rat with acute myocardial infarction and the role of insulin-like growth factor-1

BACKGROUND AIMS We investigated bone marrow stromal cell (BMSC) transplantation combined with angiotensin-converting enzyme inhibitor (ACEI) treatment in acute myocardial infarction (AMI) and the role of insulin-like growth factor-1 (IGF-1). METHODS AMI models were established in Sprague-Dawley rats by ligation of the left anterior descending coronary artery and grouped into blank control (BC), ACEI treatment (ACEI), BMSC transplantation (BMSC) and BMSC transplantation plus ACEI (combined). Perindopril (2.5 mg/kg) was administered by gavage to ACEI and combined groups from the day after AMI. BMSC (2 × 10(8)) were injected into the border of the MI area a week later in the BMSC and combined groups. RESULTS After 4 weeks, hemodynamics in the BMSC and combined groups were significantly improved (P < 0.05 versus BC), with the greatest improvement in the combined group (P < 0.05). In addition, an increased number of BMSC survived in the combined group (P < 0.05 versus BMSC). A proportion of BMSC was positive for troponin T, as detected by immunofluorescence. The number of apoptotic cardiomyocytes was decreased in the BMSC and ACEI groups, and even further in the combined group (P < 0.05). IGF-1 expression was up-regulated in the BMSC and combined groups (P < 0.05 versus BC), but not in the ACEI group. B cell lymphoma-2 (Bcl-2) expression was up-regulated in the ACEI, BMSC and combined groups, with the highest expression in the combined group (P < 0.05). CONCLUSIONS Our results show that BMSC engrafted in AMI can survive well and secrete IGF-1 and preserve cardiac function significantly. These data suggest that BMSC transplantation inhibits apoptosis of cardiomyocytes by up-regulation of Bcl-2 expression in the myocardium, and this effect might be sensitized by ACEI.

Amlodipine suppresses Ang-II-induced endothelium dysfunction by diminishing ROCK1 expression

Abstract Objective: To investigate the effects and mechanisms of amlodipine therapy on endothelium dysfunction induced by angiotensin-II (Ang-II) stimulation. Methods: Human umbilical vein endothelial cells (HUVECs) were used and divided into five groups: Blank control, Ang-II (10−6 mol/L), levorotatory amlodipine (5 × 10−6 mol/L) + Ang-II (10−6 mol/L), dextrorotatory amlodipine (5 × 10−6 mol/L) + Ang-II (10−6 mol/L) and racemic amlodipine (5 × 10−6 mol/L) + Ang-II (10−6 mol/L) groups. Twenty-four hours later, HUVECs were collected for evaluating endothelial nitric oxide synthase (eNOS), p-eNOS, rho-associated kinase 1 (ROCK1), Bcl-2 and Bax expressions. Nitric oxide (NO) concentration within endothelium was also detected. Flow cytometry was conducted to assess HUVECs apoptosis. Results: With 24 hours of Ang-II stimulation, compared to blank control group, expressions of eNOS and p-eNOS and NO production were significantly reduced in Ang-II group (p < 0.05), while adding amlodipine-protected HUVECs from dysfunction induced by Ang-II. In contrast, ROCK1 expression was promoted in Ang-II group (p < 0.05). However, the expression of ROCK1 in each enantiomer of amlodipine group was significantly decreased (p < 0.05). Compared to levorotatory amlodipine group, the magnitude of ROCK1 diminishment in dextrorotatory amlodipine group was more profound (p < 0.05). The pro-survival protein (Bcl-2) was significantly upregulated, while the pro-apoptotic protein (Bax) was significantly downregulated in three amlodipine groups compared to Ang-II group. Flow cytometry revealed that amlodipine therapy could protect HUVECs from apoptosis, and no significant difference between three amlodipine groups was observed. Conclusion: Amlodipine could suppress Ang-II-induced endothelial dysfunction and apoptosis through diminishing ROCK1 expression.

Association of N-terminal pro brain natriuretic peptide and impaired aortic elastic property in hypertensive patients.

BACKGROUND N-terminal pro brain natriuretic peptide (NT-proBNP) is closely related to risk stratification in many cardiovascular diseases. The objective of this study was to evaluate the association of NT-proBNP and impaired aortic elastic property in hypertensive patients. METHODS One hundred fifty-five hypertensive patients without obvious cardiac dysfunction were included and divided in tertiles based on their NT-proBNP concentration. Eighty-six normotensive healthy volunteers were also enrolled as controls. All subjects underwent Doppler echocardiography to assess cardiac parameters and aortic distensibility index. Plasma NT-proBNP was measured by electrochemiluminescence. RESULTS The parameters of aortic elastic property were decreased and NT-proBNP was significantly increased in hypertensive patients compared with controls (all P<0.05). Among hypertensive patients, higher NT-proBNP tertiles were associated with larger systolic and diastolic aortic diameters, longer deceleration time of the E wave velocity (DT) and isovolumic relaxation time; decreased E/A ratio and more percent of diastolic dysfunction. The parameters of aortic elastic property showed stepwise decreases from the first tertiles to the third tertiles (P<0.05). Multiple linear regression analysis showed that concentrations of NT-proBNP were significantly correlated with age and impaired aortic distensibility. CONCLUSIONS NT-proBNP is a marker for impaired aortic elastic property in hypertensive patients. Measurement of NT-proBNP could be indicated in hypertensive patients for further risk stratification.