ABSTRACT
Diabetes is associated with an increased risk of cardiovascular disease. A decrease in the number and functionality of endothelial progenitor cells (EPCs) leads to reduced endothelial repair and the development of cardiovascular disease. The aim of the present study was to explore the effect and underlying mechanisms of nuclear factor erythroid 2related factor 2 (Nrf2) on EPC dysfunction caused by diabetic mellitus. The biological functions of EPCs in streptozotocininduced diabetic mice were evaluated, including migration, proliferation, angiogenesis and the secretion of vascular endothelial growth factor (VEGF), stromalderived growth factor (SDF) and nitric oxide (NO). Oxidative stress levels in diabetic EPCs were also assessed by detecting intracellular reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA). EPC senescence was evaluated by measuring p16 and bgal expression and observing the senescenceassociated secretory phenotype. In addition, the function of EPCs and level of oxidative stress were assessed following Nrf2 silencing or activation. Nrf2 silencing resulted in a decrease of EPC biological functions, accelerated cell senescence and increased oxidative stress, as indicated by ROS and MDA upregulation accompanied with decreased SOD activity. Furthermore, Nrf2 silencing inhibited migration, proliferation and secretion in EPCs, while it increased oxidative stress and cell senescence. Nrf2 activation protected diabetic EPCs against the effects of oxidative stress and cell senescence, ameliorating the biological dysfunction of EPCs derived from mice with diabetes. In conclusion, Nrf2 overexpression protected against oxidative stressinduced functional damage in EPCs derived from diabetic mice by regulating cell senescence.
Subject(s)
Diabetes Mellitus, Experimental/metabolism , Endothelial Progenitor Cells/cytology , Endothelial Progenitor Cells/metabolism , NF-E2-Related Factor 2/metabolism , Animals , Cell Movement/physiology , Cells, Cultured , Cellular Senescence/physiology , Diabetes Mellitus, Experimental/genetics , Male , Malondialdehyde/metabolism , Mice , Mice, Inbred C57BL , Nitric Oxide/metabolism , Oxidative Stress/physiology , Reactive Oxygen Species/metabolism , Superoxide Dismutase/metabolism , Vascular Endothelial Growth Factor A/metabolismABSTRACT
AIM: To investigate the effects of depression and anxiety on health-related quality of life (QoL) in gastroesophageal reflux disease (GERD) patients and those suffering from cardiac (CCP) and noncardiac (NCCP) chest pain in Wuhan, China. METHODS: In this cross-sectional study, a total of 358 consecutive patients with GERD were enrolled in Wuhan, China, of which 176 subjects had complaints of chest pain. Those with chest pain underwent coronary angiography and were divided into a CCP group (52 cases) and NCCP group (124 cases). Validated GERD questionnaires were completed, and the 36-item Short-Form Health Survey and Hospital Anxiety/Depression Scale were used for evaluation of QoL and psychological symptoms, respectively. RESULTS: There were similar ratios and levels of depression and anxiety in GERD with NCCP and CCP. However, the QoL was obviously lower in GERD with CCP than NCCP (48.34 ± 17.68 vs 60.21 ± 20.27, P < 0.01). In the GERD-NCCP group, rather than the GERD-CCP group, the physical and mental QoL were much poorer in subjects with depression and/or anxiety than those without anxiety or depression. Anxiety and depression had strong negative correlations with both physical and mental health in GERD-NCCP (all P < 0.01), but only a weak relationship with mental components of QoL in GERD-CCP. CONCLUSION: High levels of anxiety and depression may be more related to the poorer QoL in GERD patients with NCCP than those with CCP. This highlights the importance of evaluation and management of psychological impact for improving QoL in GERD-NCCP patients.
Subject(s)
Anxiety/complications , Chest Pain/complications , Depression/complications , Gastroesophageal Reflux/complications , Quality of Life , Stress, Psychological/complications , Adult , Aged , Anxiety/epidemiology , Chest Pain/epidemiology , China/epidemiology , Comorbidity , Coronary Angiography , Cross-Sectional Studies , Depression/epidemiology , Female , Gastroesophageal Reflux/psychology , Humans , Male , Middle Aged , Stress, Psychological/epidemiology , Surveys and QuestionnairesABSTRACT
OBJECTIVE: Drug-induced liver damage is a potential complication from using many drugs. The aim of our study was to analyze the etiology and clinical features of drug-induced liver damage, in order to draw more attention to this problem. METHODS: Two hundred and seventy-six cases over a 5-year period in Jiangsu Province Hospital were retrospectively analyzed. RESULTS: A variety of drugs, including traditional Chinese medicines (26.1% of our total cases) and anticancer drugs (17%) caused liver damage. The main clinical manifestations of it were fatigue, nausea, vomiting and jaundice. In 88% of our cases the symptoms were relieved or completely disappeared, but there was still a 5.1% mortality rate. CONCLUSIONS: The clinical features of drug-induced liver damage are of no specificity, and the mortality of it is not low. Liver function should be monitored when suspected drugs are prescribed.
