In situ SAXS probing the evolution of the precursors and onset of nucleation of ZnSe colloidal semiconductor quantum dots.

The whole evolution processes, from precursors to quantum dots (QDs), were in situ investigated by SAXS and UV-vis. Diphenylphosphine (HPPh2) accelerates the dissolution of zinc oleate lamellar mesophase in the presence of selenide tri-n-octylphosphine (SeTOP) at a low temperature of 40 °C via the equilibrium of SeTOP + HPPh2 ⇔ SePPh2H + TOP.

Exendin-4 protects HUVECs from tunicamycin-induced apoptosis via inhibiting the IRE1a/JNK/caspase-3 pathway.

Purpose: The abnormal increase of apoptosis of endothelial cells induced by endoplasmic reticulum stress is a significant factor for vascular disease, especially for atherosclerosis. Protecting endothelial cells from endoplasmic reticulum stress is a crucial strategies to combate these diseases. The goal of this study was to explore the effect of Exendin-4, a glucagon-like peptide-1 receptor agonist, on tunicamycin-induced apoptosis in human umbilical vein endothelial cells.

[The Effect of recombinant adiponectin on apoptosis induced by t-BHP in human umbilical vein endothelial cells].

Objective: To investigate the protective effect and possible mechanism of recombinant adiponectin on apoptosis in Human Umbilical Vein Endothelial Cells (HUVECs) induced by tert-butyl hydroperoxide (t-BHP).

Methods: HUVECs were cultured in vitro and apoptosis was induced by t-BHP. On this basis, HUVECs were transfected with adenovirus carrying adiponectin prior to exposure to t-BHP, to further explore the protective effect of adiponectin on apoptosis induced by t-BHP.

Liraglutide prevents beta-amyloid-induced neurotoxicity in SH-SY5Y cells via a PI3K-dependent signaling pathway.

Objectives: The aim of the study was to investigate the effects of the GLP-1 analog liraglutide on beta-amyloid (Aβ)-induced neurotoxicity in the human neuroblastoma cell line SH-SY5Y and study the underlying mechanisms.

Methods: Cultured SH-SY5Y cells in vitro were randomly divided into normal control group, beta-amyloid (Aβ) group (20, 40, and 80 uM), and liraglutide pre-treatment group (10, 100, and 200 nM). Cell viability was determined by CCK-8 and lactate dehydrogenase (LDH).

Exendin-4 Protects MIN6 Cells from t-BHP-Induced Apoptosis via IRE1-JNK-Caspase-3 Signaling.

Objectives. This study aimed to explore the effect of exendin-4 on t-BHP-induced apoptosis in pancreatic β cells and the mechanism of action. Methods.

[Oxidative damage to the endoplasmic reticulum stress pathway of apoptosis-related molecules expression in MIN6 cell].

Aim: Through a third-butyl hydrogen peroxide (t-BHP) induced apoptosis in pancreatic islet β-cells to study the oxidative damage induced endoplasmic reticulum stress-JNK pathway of apoptosis related molecules in vitro.

Methods: Mouse insulinoma(MIN6) cells was administered with t-BHP which were cultured in vitro. Choosing medicine with different concentrations(0-400 μmol/L)and time periods(0-8 h)to establish the cells apoptosis model.

[The chronic effect of palmitic acid on apoptosis of pancreatic islet beta-cells and the mechanism].

Aim: To investigate the chronic effect of palmitic acid (PA) on apoptosis of pancreatic islet beta-cells and the possible mechanism.

Methods: Insulinoma cell line (MIN6 cells) were used in this study. After being incubated in PA (0.

Exendin-4 protects murine pancreatic β-cells from dexamethasone-induced apoptosis through PKA and PI-3K signaling.

Aims: To explore the effect and mechanism of exendin-4 on dexamethasone-induced apoptosis in pancreatic β-cells.

Methods: Murine MIN6 pancreatic β-cells were treated with dexamethasone (100 nmol/l) over 48h following pretreatment with exendin-4 (100 nmol/l). Cell viability was determined using an MTT assay.

[Dexamethasone-induced apoptosis of murine MIN6 pancreatic beta-cells and its effect on AKT phosphorylation].

This study is to investigate the effect of dexamethasone on cell apoptosis of murine MIN6 pancreatic beta-cells, and to investigate the mechanism of dexamethasone-dependent cell apoptosis. The cell apoptosis model was established by choosing the murine MIN6 pancreatic beta-cells, which was cultured in vitro and induced by dexamethasone. The morphology of the cell apoptosis was observed through fluorescence microscopic analysis after Hochest/PI staining and flow cytometric assay after Annexin-V/PI staining.