Lipophilic ferulic acid derivatives protect PC12 cells against oxidative damage via modulating β-amyloid aggregation and activating Nrf2 enzymes.

Ferulic acid (FA) has been shown to have a neuroprotective effect on Alzheimer's disease induced by amyloid-beta (Aβ) neurotoxicity. This work aims to ascertain the structure-activity relationship of FA and its alkyl esters (FAEs) for evaluating the antioxidant activities in PC12 cells and Aβ aggregation inhibitory activities in vitro, as well as the signaling mechanisms against oxidative stress elicited by Aβ in PC12 cells. Our data showed that alterations in the subcellular localization and cytotoxicity of FAEs caused by the lipophilicity of FA were crucial when evaluating their antioxidant capacities.

Electric field exposure promotes epithelial‑mesenchymal transition in human lens epithelial cells via integrin β1‑FAK signaling.

Electric field (EF) exposure can affect the elongation, migration, orientation, and division of cells. The present study tested the hypothesis that EF may also affect epithelial‑mesenchymal transition (EMT) in lens epithelial cells and that this effect may be an important inducer in the pathological process of posterior capsule opacification (PCO). Human lens epithelial (HLE)‑B3 cells were exposed to an EF.

E-26 Transformation-specific Related Gene Expression and Outcomes in Cytogenetically Normal Acute Myeloid Leukemia: A Meta-analysis.

Background: The E-26 transformation-specific related gene (ERG) is frequently expressed in cytogenetically normal acute myeloid leukemia (CN-AML). Herein, we performed a meta-analysis to investigate the relationship between the prognostic significance of ERG expression and CN-AML.

Methods: A systematic review of PubMed database and other search engines were used to identify the studies between January 2005 and November 2016.

KIT and BRAF heterogeneous mutations in gastrointestinal stromal tumors after secondary imatinib resistance.

Background And Aims: Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumor of the digestive tract and characterized by expression of KIT protein. Imatinib is the frontline therapy for metastatic and unresectable GIST patients showing clinical responses in 80 % of cases. Despite the often long-lasting clinical benefit seen in most patients treated with imatinib, many will eventually suffer disease progression.

Andrographolide sodium bisulfate-induced apoptosis and autophagy in human proximal tubular endothelial cells is a ROS-mediated pathway.

Background And Aims: The nephrotoxic mechanisms of andrographolide sodium bisulfate (ASB) remain largely unknown. This study attempted to explore the mechanism of ASB-induced nephrotoxicity using human proximal tubular endothelial cells (HK-2).

Methods: For this study HK-2 cells were treated with rising concentrations of ASB.

Crystal structures, interactions with biomacromolecules and anticancer activities of Mn(II), Ni(II), Cu(II) complexes of demethylcantharate and 2-aminopyridine.

Three novel transition metal complexes (Hapy)(2)[M(DCA)(2)]·6H(2)O (M = Mn(II) (1), Ni(II) (2), Cu(II) (3); DCA = demethylcantharate, 7-oxabicyclo[2.2.1]heptane-2,3-dicarboxylate, C(8)H(8)O(5); Hapy = 2-aminopyridine acid, C(5)H(7)N(2)) were synthesized and characterized by elemental analysis, infrared spectra, thermogravimetric analysis and X-ray diffraction.

Aquaporin-4 deficiency attenuates acute lesions but aggravates delayed lesions and microgliosis after cryoinjury to mouse brain.

Objective: To determine whether aquaporin-4 (AQP4) regulates acute lesions, delayed lesions, and the associated microglial activation after cryoinjury to the brain.

Methods: Brain cryoinjury was applied to AQP4 knockout (KO) and wild-type mice. At 24 h and on days 7 and 14 after cryoinjury, lesion volume, neuronal loss, and densities of microglia and astrocytes were determined, and their changes were compared between AQP4 KO and wild-type mice.

Mast cell degranulation induced by chlorogenic acid.

Aim: To investigate the mechanism of chlorogenic acid (CA)-induced anaphylactoid reactions.

Methods: Degranulation of peritoneal mast cells was assayed by using alcian blue staining in guinea pigs, and the degranulation index (DI) was calculated. CA-induced degranulation of RBL-2H3 cells was also observed and assayed using light microscopy, transmission electron microscopy, flow cytometry, and beta-hexosaminidase release.

Synthesis, characterization, DNA-binding and antiproliferative activity of Nd(III) complexes with N-(nitrogen heterocyclic) norcantharidin acylamide acid.

Three novel complexes [Nd(L)(NO3)(H2O)2].NO(3).2H2O (HL1 = N-pyrimidine norcantharidin acylamide acid, C12H13N3O4; HL2 = N-pyridine norcantharidin acylamide acid, C13H14N2O4; HL3 = N-phenyl norcantharidin acylamide acid, C14H15NO4) were synthesized.

[Cysteinyl leukotriene receptor 1 antagonist pranlukast modulates differentiation of SK-N-SH cells].

Objective: To determine whether cysteinyl leukotriene receptor agonist LTD(4) and cysteinyl leukotriene receptor 1 (CysLT(1)) antagonist pranlukast affect the differentiation of human neuroblastoma SK-N-SH cells.

Methods: SK-N-SH cell morphological changes induced by LTD(4), pranlukast and LTD(4) + pranlukast were observed with retinoid acid (RA) as the positive control. The expressions of CysLT(1) and CysLT(2) receptors were detected by immunoblotting analysis, and the expression of microtubule-associated protein-2 (MAP-2), a neuron marker, was detected by fluorescent immunostaining.

Astilbic acid induced COLO 205 cell apoptosis by regulating Bcl-2 and Bax expression and activating caspase-3.

Aim: To investigate the effect of astilbic acid (3beta, 6beta-dihydroxyolean-12-en-27-oic acid, AA) on human colorectal carcinoma COLO 205 cell proliferation and apoptosis.

Methods: Proliferation of COLO 205 cells was measured by MTT assay. Content of DNA in COLO 205 cell was measured by modified diphenylamine assay.