Search Results
You are looking at 1 - 2 of 2 items for :
- Author or Editor: L. Zhong x
- Medical and Health Sciences x
- Refine by Access: All Content x
This paper proposed a relative value method for measuring the indicators of cardiac reserve and investigated the application on monitoring and evaluating cardiac function for pregnant women. A heart sound sensor is placed at the precordial region to detect phonocardiogram. In order to access the cardiac reserve mobilization level during pregnancy, the cardiac reserve indicators of 1,683 normal pregnant women, 96 abnormal cases with different obstetric complications and 624 non-pregnant women were measured, analyzed and compared. The result shows that the differences between the indicators of pregnant and non-pregnant women were significant (p < 0.05). The ratio of diastolic to systolic duration (D/S) was obviously declined with the increase of gestational weeks and the occurrence of obstetric complication. This very encouraging result indicates that the D/S can be used as an indicator for evaluating the cardiac safety of parturition, which provides a reference for cardiac safety assessment of pregnant women.
Abstract
Although the use of aspirin has substantially reduced the risks of cardiovascular events and death, its potential mechanisms have not been fully elucidated. In a previous study, we found that aspirin triggers cellular autophagy. In the present study, we aimed to determine the protective effects of aspirin on human coronary artery endothelial cells (HCAECs) and explore its underlying mechanisms. HCAECs were treated with oxidized low-density lipoprotein (ox-LDL), angiotensin II (Ang-II), or high glucose (HG) with or without aspirin stimulation. The expression levels of endothelial nitric oxide (NO) synthase (eNOS), p-eNOS, LC3, p62, phosphor-nuclear factor kappa B (p-NF-κB), p-p38 mitogen-activated protein kinase (p-p38 MAPK), and Beclin-1 were detected via immunoblotting analysis. Concentrations of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured via ELISA. NO levels were determined using the Griess reagent. Autophagic flux was tracked by tandem mRFP-GFP-tagged LC3. Results showed that aspirin increased eNOS level and reduced injury to the endothelial cells (ECs) caused by ox-LDL, Ang-II, and HG treatment in a dose-dependent manner. Aspirin also increased the LC3II/LC3I ratio, decreased p62 expression, and enhanced autophagic flux (autophagosome and autolysosome puncta) in the HCAECs. p-NF-κB and p-p38 mitogen-activated protein kinase inhibition, sVCAM-1 and sICAM-1 secretion, and eNOS activity promotion by aspirin treatment were found to be dependent on Beclin-1. These results suggested that aspirin can protect ECs from ox-LDL-, Ang-II-, and HG-induced injury by activating autophagy in a Beclin-1-dependent manner.
