Copper (II) Species with Improved Anti-Melanoma and Antibacterial Activity by Inclusion in ß-Cyclodextrin.

To improve their biological activity, complexes [Cu(bipy)(dmtp)2(OH2)](ClO4)2·dmtp (1) and [Cu(phen)(dmtp)2(OH2)](ClO4)2·dmtp (2) (bipy 2,2'-bipyridine, phen: 1,10-phenantroline, and dmtp: 5,7-dimethyl-1,2,4-triazolo [1,5-a]pyrimidine) were included in ß-cyclodextrins (ß-CD). During the inclusion, the co-crystalized dmtp molecule was lost, and UV-Vis spectra together with the docking studies indicated the synthesis of new materials with 1:1 and 1:2 molar ratios between complexes and ß-CD. The association between Cu(II) compounds and ß-CD has been proven by the identification of the components' patterns in the IR spectra and powder XRD diffractograms, while solid-state UV-Vis and EPR spectra analysis highlighted a slight modification of the square-pyramidal stereochemistry around Cu(II) in comparison with precursors. The inclusion species are stable in solution and exhibit the ability to scavenge or trap ROS species (O2·- and HO·) as indicated by the EPR experiments. Moreover, the two inclusion species exhibit anti-proliferative activity against murine melanoma B16 cells, which has been more significant for (2)@ß-CD in comparison with (2). This behavior is associated with a cell cycle arrest in the G0/G1 phase. Compared with precursors, (1a)@ß-CD and (2a)@ß-CD exhibit 17 and 26 times more intense activity against planktonic Escherichia coli, respectively, while (2a)@ß-CD is 3 times more active against the Staphylococcus aureus strain.

Bacterial Cellulose-Carboxymethylcellulose Composite Loaded with Turmeric Extract for Antimicrobial Wound Dressing Applications.

Bacterial cellulose (BC) is a biopolymer whose properties have been intensively studied, especially for biomedical applications. Since BC has no antimicrobial activity, it is necessary to use bioactive substances for developing wound healing applications. Another drawback of BC is the loss if its water retention capacity after dehydration. In order to overcome these problems, carboxymethyl cellulose (CMC) and turmeric extract (TE) were selected for the preparation of BC composites. Citric acid (CA) was used as the crosslinking agent. These composites were tested as potential antimicrobial wound dressing materials. TE-loaded BC-CMC composites were characterized in terms of their morphology, crystallinity, and thermal behavior. Swelling tests and curcumin-release kinetic analysis were also performed. All the composites tested had high swelling degrees, which is an advantage for the exudate adsorption from chronic wounds. The antibacterial potential of such composites was tested against Escherichia coli (E. coli), Staphylococcus aureus (S. aureus), and Candida albicans (C. albicans). The in vitro cytotoxicity toward L929 fibroblast cells was studied as well. The obtained results allow us to recommend these composites as good candidates for wound dressing applications.

Ca2+ homeostasis in brain microvascular endothelial cells.

Blood brain barrier (BBB) is formed by the brain microvascular endothelial cells (BMVECs) lining the wall of brain capillaries. Its integrity is regulated by multiple mechanisms, including up/downregulation of tight junction proteins or adhesion molecules, altered Ca2+ homeostasis, remodeling of cytoskeleton, that are confined at the level of BMVECs. Beside the contribution of BMVECs to BBB permeability changes, other cells, such as pericytes, astrocytes, microglia, leukocytes or neurons, etc. are also exerting direct or indirect modulatory effects on BBB. Alterations in BBB integrity play a key role in multiple brain pathologies, including neurological (e.g. epilepsy) and neurodegenerative disorders (e.g. Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis etc.). In this review, the principal Ca2+ signaling pathways in brain microvascular endothelial cells are discussed and their contribution to BBB integrity is emphasized. Improving the knowledge of Ca2+ homeostasis alterations in BMVECa is fundamental to identify new possible drug targets that diminish/prevent BBB permeabilization in neurological and neurodegenerative disorders.