The concept that flavonoids exert cardioprotection against myocardial ischemia-reperfusion (I/R) injury has been acknowledged by a large body of evidence. However, recent studies reported cardiotoxic effects of certain flavonoids, while the underlying mechanisms have remained largely elusive. Flavonoids have been demonstrated to activate aryl hydrocarbon receptor (Ahr), which is implicated in an array of cell signaling processes. The present study examined the cardioprotective roles of quercetin (Qu) and β-naphthoflavone (β-NF) against I/R injury and explored whether the underlying mechanism proceeds via molecular signaling downstream of Ahr. An oxygen glucose deprivation/reoxygenation (OGD/R) model of I/R was established in myocardial H9c2 cells in the absence or presence of Qu or β-NF. Qu as well as β-NF reversed OGD/R-induced overproduction of reactive oxygen species by increasing the anti-oxidative capacity of the cells and protected them from lethal injury, as demonstrated by a decreased cell death rate, lactate hydrogenase leakage and caspase-3 activity as determined by flow cytometry, colorimetric assay and western blot analysis, respectively. Immunocytochemistry, co-immunoprecipitation and western blot assays collectively revealed that Qu and β-NF engendered the translocation of Ahr from the cytoplasm into the cell nucleus, where binding of Ahr with the Ahr nuclear translocator (ARNT) blocked its binding to hypoxia-inducible factor (HIF)-1α, which inhibited the cardioprotection of HIF-1α, including the induction of nitric oxide (NO) and inhibition of vascular endothelial growth factor (VEGF) production. Ahr knockdown recovered the binding of ARNT to HIF-1α and the generation of NO and VEGF. The results of the present study suggested a dual character of Qu and β-NF in the process of myocardial I/R.

Ultrasound synergized a combined regime and sonochemotherapy was a measure to suppress cancer spread.

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Sepsis is characterized by injury to the microvasculature and the microvascular endothelial cells, leading to barrier dysfunction. However, the specific role of injury in septic endothelial barrier dysfunction remains to be elucidated. In the present study, it was hypothesized that endothelial cell inflammatory injury is likely required for barrier dysfunction under septic conditions in vitro. 2,3,5,4'‑Tetrahydroxystilbene‑2‑O‑β‑D‑glucoside (TSG), a compound extracted from Chinese herbs, is able to inhibit the inflammatory injury of septic‑serum in endothelial cells. In the present study, cell viability was assayed by CCK‑8 method; mRNA and protein expression was identified by RT‑qPCR, western blot or Elisa, respectively and the production of reactive oxygen species was observed by a fluorescence microscope. The present study indicated that septic serum significantly decreased the cell viability of pulmonary aortic endothelial cells (PAECs) following co‑cultivation for 6 h, which occurred in a time‑dependent manner. TSG notably increased the viability of PAECs in a time‑ and concentration‑dependent manner. Further investigations revealed that septic serum increased the secretion of interleukin (IL)‑1β, IL‑6 and C‑reactive protein in PAECs, whereas pretreatment with TSG significantly decreased the secretion of these inflammatory factors. These data indicated that septic serum increased inflammatory injury to the PAECs, and TSG decreased this injury via the reactive oxygen species‑mitogen‑activated protein kinase‑nuclear factor‑κB signaling pathway.

Previous studies have shown that microRNA (miR)-125b plays important roles in several human cancer types. The aim of the present study was to analyze the potential roles of miR-125b in papillary thyroid carcinoma (PTC). It was found that miR-125b was downregulated in PTC and its expression was affected by clinical stages. Glucose transporter 1 (GLUT1) was upregulated in PTC and was negatively correlated with miR-125b. In PTC cells, overexpression of miR-125b suppressed glucose uptake and downregulated GLUT1. Furthermore, GLUT1 overexpression reduced the effects of miR-125b overexpression on glucose uptake. Moreover, miR-125b overexpression suppressed PTC cell proliferation. GLUT1 overexpression promoted the proliferation of PTC cells and reduced the effects of miR-125b overexpression on cancer cell proliferation. Overall, miR-125b decreased glucose uptake in PTC cells by downregulating GLUT1.