LncRNA ZEB1-AS1 knockdown alleviates oxidative low-density lipoprotein-induced endothelial cell injury via the miR-590-5p/HDAC9 axis.

Oxidative low-density lipoprotein (ox-LDL) is thought to induce vascular endothelial cell injury, which contributes to the aetiopathogenesis of atherosclerosis (AS). Several previous reports have identified that lncRNA ZEB1-AS1 participates in the regulatory mechanisms of endothelial cell injury, but the potential interaction mechanism between ZEB1-AS1 and miR-590-5p in ox-LDL-induced endothelial cell damage is not clear. ZEB1-AS1 and miR-590-5p expression were tested by quantitative real-time polymerase chain reaction (qRT-PCR) in ox-LDL-treated endothelial cells. The proliferation and apoptosis were determined by MTT and Annexin V/PI double-staining assay, respectively. The protein expression of HDAC9, tumor necrosis factor α (TNF-α), cleaved caspase-3, and cleaved PARP were measured by western blot analysis. Dual-luciferase reporter and RIP assays affirmed the functional targets of ZEB1-AS1. ZEB1-AS1 expression was upregulated in ox-LDL-treated HUVECs, and miR-590-5p was lessened in a dose- or time-depended manner, respectively. Knockdown of ZEB1-AS1 facilitated ox-LDL-treated endothelial cell proliferation and inhibited cell apoptosis. Moreover, miR-590-5p was directly targeted via ZEB1-AS1 in ox-LDL-treated HUVECs. ZEB1-AS1 silencing attenuated ox-LDL-induced cell injury via regulation of miR-590-5p expression. Furthermore, HDAC9 reversed the influence of miR-590-5p on propagation and apoptosis of ox-LDL-induced endothelial cells. Knockdown of ZEB1-AS1 alleviates ox-LDL-induced endothelial cell injury by regulating the miR-590-5p/HDAC9 axis.

A narrative review of the research status of exosomes in cardiovascular disease.

OBJECTIVE: Cardiovascular diseases (CVDs) are a major health problem worldwide, and medical workers are actively seeking new and effective methods to predict and treat CVDs. Exosomes are secreted by a variety of cells and exist in a variety of body fluids and tissues. Exosomes play an important role in signal transmission between cells and participate in various physiological and pathological activities of the organism. We sought to identify new diagnosis and treatment ideas related to the application of exosomes in CVDs. BACKGROUND: In the cardiovascular system, exosomes are related to endothelial cells, cardiomyocytes, vascular cells, stem cells, and progenitor cells. They can promote angiogenesis, inhibit ventricular remodeling, improve heart function, inhibit local inflammation, and regulate immune responses. They play an important role in the development, injury, and disease of the cardiovascular system. However, as an emerging field, researchers are still trying to fully understand the role of exosomes and their mechanisms in mediating heart repair. METHODS: We searched the China National Knowledge Infrastructure, Wanfang Database, PubMed, and Web of Science databases to find relevant articles. The Chinese and English search terms were "exosomes" and "cardiovascular disease". Ultimately, 96 articles were included in the review. CONCLUSIONS: Exosomes play an important role in the cardiovascular system, and are widely involved in the occurrence and development of CVDs, such as atherosclerosis (AS), acute myocardial infarction (AMI), heart failure (HF), myocardial ischemia-reperfusion (I/R) injury, pulmonary hypertension (PH), and diabetic heart disease. In this review, we summarize research on exosomes in relation to the mechanisms, diagnoses and treatments of CVDs. We also provide new diagnosis and treatment ideas, and promote the clinical application of exosomes.

Identification of lncRNA-mRNA regulatory network associated with isolated systolic hypertension and atherosclerotic cerebral infarction.

BACKGROUND: Increasingly, evidence has shown that long non-coding RNAs (lncRNAs) play an important role in isolated systolic hypertension (ISH). However, a systematic lncRNA-messenger RNA (mRNA) regulatory network is still absent in isolated systolic hypertension and atherosclerotic cerebral infarction patients (ISH & ACI). This research aimed to establish a lncRNA-mRNA co-expression network in patients with ISH & ACI, to probe into the potential functions of lncRNA in such patients. METHODS: Expression profiles of lncRNA and mRNAs were collected and compared, from 8 patients with ISH and 8 patients with ISH & ACI by RNA-seq data. Differentially expressed lncRNAs and mRNAs were screened out via high-throughput sequencing in the plasma of ISH/ACI patients and control ISH patients. Then, a lncRNA-mRNA interaction network was built using the Pearson correlation coefficient by Cytoscape software. The expression levels of the hub genes and lncRNAs were verified by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) in another 10 ISH/ACI patients and 10 control patients. This study was approved by the responsible institutional review board (IRB) and informed consent was provided by participants. RESULTS: A total of 2,768 differentially expressed lncRNAs and 747 differentially expressed mRNAs were identified. We identified two hub genes (CD226 and PARVB) and 11 lncRNAs in the lncRNA-mRNA interaction network. The results of qRT-PCR and cell assay verified that lncRNAs ENST00000590604 and CD226 are highly expressed in patients of ISH & ACI. Further, CD226 was associated with vascular endothelial cells growth and stability through the platelet activation and focal adhesion pathway. CONCLUSIONS: We established a novel mRNA-lncRNA interaction network. The lncRNAs ENST00000590604 and CD226 might be the potential biomarkers of ISH & ACI.

A health education model based on knowledge, attitude, and practice used as adjunct therapy for metabolic syndrome complicated with acute pancreatitis: A case report.

Herein, a relatively rare case is reported in which a knowledge, attitude, and practice (KAP) health education model was applied in a young female patient with metabolic syndrome (MS) and acute pancreatitis (AP), with a satisfactory effect. The purpose of this report is to provide a reference for a viable health education program in clinical practice for intervention of MS with concurrent AP in the absence of clinical trials. The patient's unhealthy lifestyle led to obesity, diabetes mellitus, severe fatty liver, hyperlipidemia, and AP. We used a KAP health education model in a nursing intervention and evidence-based multidisciplinary cooperation to develop a personalized diet, exercise plan, education plan, and continuous care of the patient after discharge from the hospital. Within 2 months, the patient achieved weight loss, stable blood lipids, controlled blood sugar levels, and decreased glycated hemoglobin level from 9.0% to 5.4%. This KAP-based health education model has clinical importance as an intervention for lifestyle modification in patients with MS and AP. This approach can be adopted to help other patients to effectively control and prevent the recurrence of diseases.

Ebselen protects rat hearts against myocardial ischemia-reperfusion injury.

Ebselen is an organoselenium compound that has demonstrated potent antioxidant and anti-inflammatory effects in previous studies. The present study was conducted to evaluate the effect of ebselen on myocardial ischemia-reperfusion (I/R) injury in a rat model and to elucidate the related mechanisms. Myocardial infarct size was assessed using triphenyltetrazolium chloride staining. Myocardial injury was evaluated according to the histopathological and ultrastructural alterations of rat hearts and the serum activity levels of cardiac enzymes, including creatine kinase (CK), CK-MB isoenzyme and lactate dehydrogenase (LDH). Cardiomyocyte apoptosis was detected using the terminal dUTP nick end-labelling (TUNEL) assay. In addition, the expression of apoptosis-associated proteins was measured using western blot analysis. In heart tissue specimens the activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx), and levels of malondialdehyde (MDA) and protein carbonyl (PC) were also detected. The results indicated that ebselen reduced I/R-induced increase in myocardial infarct size and prevented the I/R-induced decreases in ejection fraction and fractional shortening. Further of note, ebselen improved I/R-induced rat heart injury. This was indicated by attenuation of histological and ultrastructural changes; reduction of serum CK, CK-MB and LDH activity levels; and decreased cell apoptosis on TUNEL staining, which was verified by decreased expression of cleaved (C)-Caspase-8, C-Caspase-3, B-cell lymphoma 2 (Bcl-2)-associated X protein and C-PARP, and increased expression of Bcl-2. Additionally, SOD and GPx activity levels were significantly higher, while MDA and PC levels were significantly lower in the ebselen + I/R group compared with in the I/R group. In conclusion, the present results suggested that ebselen serves an important role in protecting against myocardial I/R injury. The underlying mechanism may involve suppression of cardiomyocyte apoptosis and promotion of antioxidant activity.