Background/Aims: Troxerutin, also known as vitamin P4, has been commonly used in the treatment of chronic venous insufficiency (CVI) disease. However, its effect on in vivo myocardial ischemia/reperfusion (I/R) injury, a model that closely mimics acute myocardial infarction in humans, is still unknown. Methods: The myocardial I/R injury rat model was created with troxerutin preconditioning. Myocardial infarct size was evaluated by the Evans blue-TTC method. Hemodynamic parameters, including the heart rate (HR), left ventricular end-diastolic pressure (LVEDP), left ventricular systolic pressure (LVSP), maximal rate of rise in blood pressure in the ventricular chamber (+dp/dt max), and maximal rate of decline in blood pressure in the ventricular chamber (-dp/dt max) were monitored. Serum TNF-α and IL-10 were determined by ELISA kit. Cell apoptosis was detected by MTT method. Results: Troxerutin preconditioning significantly reduced myocardial infarct size, improved cardiac function, and decreased the levels of creatine kinase (CK), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) in the I/R injury rat model. The serum and mRNA levels of TNF-α and IL-10 as well as some apoptosis markers (Bax, Caspase 3) also decreased. Moreover, troxerutin pretreatment markedly increased the phosphorylation of Akt, and blocking PI3K activity by LY294002 abolished the protective effect of troxerutin on I/R injury. Conclusion: Troxerutin preconditioning protected against myocardial I/R injury via the PI3K/Akt pathway.

Several miRNAs have been demonstrated to be involved in endothelial dysfunction during atherosclerosis (AS). However, the detailed roles and underlying mechanisms of miR-34a in AS-associated endothelial cell apoptosis are far from being addressed. Apolipoprotein E-deficient (ApoE) mice fed with high-fat diet (HFD) were used as in vivo model of AS. Oxidized low-density lipoprotein (ox-LDL)-treated human aortic endothelial cells (HAECs) were applied as in vitro model of AS. The effects of miR-34a on atherosclerotic lesions were evaluated by hematoxylin-eosin (HE) and Oil Red O staining. Pecam-1 endothelial cells were isolated from the aortic arch with flow cytometry. qRT-PCR and western blot were employed to measure gene and protein expression. The effects of miR-34a on cell viability, cell cycle distribution, and apoptosis were assessed by Cell counting kit (CCK)-8 and flow cytometry analysis. The relationship between miR-34a and Bcl-2 was confirmed by online softwares, luciferase reporter assay, and RNA immunoprecipitation (RIP). miR-34a was upregulated in HFD-induced ApoE mice and ox-LDL-treated HAECs. Anti-miR-34a decreased atherosclerotic lesions and inhibited Pecam-1 endothelial cells apoptosis in HFD-induced ApoE mice. Moreover, anti-miR-34a significantly promoted cell viability, alleviated cell cycle arrest, and restrained apoptosis in ox-LDL-treated HAECs. Furthermore, Bcl-2 was identified as a target of miR-34a, and miR-34a inhibited Bcl-2 expression via binding to its 3'UTR. Rescue experiments demonstrated that Bcl-2 overexpression dramatically reversed miR-34a-mediated inhibition of cell growth and promotion of apoptosis in ox-LDL-exposed HAECs. Depletion of miR-34a facilitated endothelial cell growth and blocked apoptosis in AS by upregulating Bcl-2, offering a promising avenue for AS therapy.

Renal ischemia-reperfusion (I/R) injury can be caused by cardiac surgery, renal vascular obstruction, and kidney transplantation, mainly leading to acute kidney injury (AKI), which is complicated by lack of effective preventative and therapeutic strategies. Ghrelin has recently been reported to possess anti-inflammatory properties in several types of cells; however, little attention has been given to the role of ghrelin in I/R-induced AKI. The aim of this study is to explore the role of ghrelin in I/R-induced AKI. In this study, an I/R-induced rat AKI model and a hypoxia-induced NRK-52E cell I/R model were successfully constructed. Ghrelin expression was increased significantly in these rat and cell models. After enhancing ghrelin level by injecting exogenous ghrelin into rats or transfecting a ghrelin-pcDNA3.1 vector into renal tubular epithelial cells, we observed that I/R-induced AKI can be ameliorated by ghrelin, as shown by alterations in histology, as well as changes in serum creatinine (SCr) level, cell apoptosis, and the levels of inflammatory factors. Based on the importance of microRNA-21 (miR-21) in renal disease and the modulation effect of ghrelin on miR-21 in gastric epithelial cells, we tested whether miR-21 participates in the protective effect of ghrelin on I/R-induced AKI. Ghrelin could upregulate the PI3K/AKT signaling pathway by increasing the miR-21 level, which led to the protective effect of ghrelin on I/R-induced AKI by inhibiting the inflammatory response and renal tubular epithelial cell apoptosis. Our research identifies that ghrelin can ameliorate I/R-induced AKI by upregulating miR-21, which advances the understanding of mechanisms by which ghrelin ameliorates I/R-induced AKI.

Several authors have described anatomic variations of the aortic arch in 13% to 20% of the patients who do not have aortic disease. However, few studies have evaluated these patterns in the thoracic aortic dissection (TAD). In the authors’ knowledge, this is the first survey that specifically investigates the frequency of these variations in a broad, nonselected group of Chinese patients with aortic dissection. Furthermore, it compares this group with a group of patients without aortic disease.The objective of this study was to define the variation frequency of the aortic arch branches pattern using the tomographic studies of 525 Chinese patients with a diagnosis of TAD. The Stanford classification was used to set the site of the initial tear of the dissection. In addition, we performed an epidemiological analysis of the aortic arch anatomic variations in TAD, and its possible implications for surgical or endovascular treatment. The general hypothesis proposal asserted that Chinese patients with dissection of the aorta have a similar incidence of variations of the aortic arch to the patients without aortic disease.A retrospective study of cases and controls was carried out using the tomographic studies (CT) of all patients admitted to the First Affiliated Hospital of Zhengzhou University, located at Henan-China, with a confirmed diagnosis of aortic dissection from January 2012 until December 2014. The group of cases consisted of 525 patients: 374 men and 151 women, with a mean age of 52.27 years (range, 20–89). The average age of the patients with Stanford A and B aortic dissection was 49.46 and 53.67, respectively. The control group consisted of 525 unselected patients without TAD who underwent a CT scan of the chest due to other indications. This group consisted of 286 men and 239 women, with a mean age of 53.60 years (range, 18–89). All the patients with aneurysm or dissection were excluded from the control group. We performed a statistical analysis of demographic data.The study found 7 different patterns of the aortic arch on both groups of cases and controls. Within the 525 patients with TAD were observed 85 (16.19%) anatomical variations, while the control group showed 112 variations (21.33%); P = 0.033. The most common anatomical variant was the bovine arch, found in 62 (11.80%) cases of TAD compared with 77 (14.66%) in the control group; P = 0.172. Anatomical variations were observed in 14.32% of the patients with Stanford A dissection and 17.09% of the patients with Stanford B dissection; P = 0.425. Patients with Stanford A dissection showed the pattern of bovine arch in 23 (13.21%) of 174 cases. In contrast, the patients with Stanford B dissection showed it in 39 (11.11%) of 351 cases; P = 0.481. The anatomical variant defined as vertebral artery of direct origin of the aortic arch was more frequent in the patients with Stanford B dissection (5.12%). The patients with Stanford A dissection presented this pattern in 1.14% of the cases; P = 0.025. This study observed an increased frequency of aort...