Induced osteogenesis of mesenchymal stem cells (MSCs) may provide an important tool for bone injures treatment. Human umbilical cord and adipose tissue are routinely discarded as clinical waste and may be used as uncontroversial MSCs sources. It still remains to be verified which source of MSCs is the most suitable for bone regeneration.The aim of this research was to investigate the osteogenic potential of human MSCs derived from adipose tissue (ASCs) and Wharton’s jelly of the human umbilical cord (WJ-MSCs) differentiated under the same conditions.Osteogenic differentiation of MSCs was detected and quantified by ARS staining for calcium deposition and alkaline phosphatase (ALP) activity, osteoprotegerin (OPG), and osteocalcin (OC) secretion measurements. Under osteogenic conditions the measured ALP activity and calcium deposition were significantly higher in ASCs than in WJ-MSCs, while the OPG and OC secretion were higher in WJ-MSCs vs. ASCs. Low concentrations of OPG and high levels of OC in ASCs and WJ-MSCs, prove that these cells reached an advanced stage of the osteogenic differentiation. The levels of OC secreted by ASCs were lower than by WJ-MSCs what indicates that the differentiation process of the ASCs reached the stage when the extracellular matrix is overproduced and the down-regulation of OC begins.Both cell types, ASCs and WJ-MSCs possess potential to differentiate towards the osteogenic lineage. However, the observed differences in the levels of osteogenic markers suggest that ASCs may be better candidates for cell-based osteogenesis than WJ-MSCs.

Phytic acid (PA) has been recognized as a potent antioxidant and inhibitor of iron-catalyzed hydroxyl radical formation underin vitroandin vivoconditions. Therefore, the aim of the present study was to investigate, with the use of HPLC/MS/MS, whether PA is capable of inhibiting linoleic acid autoxidation and Fe(II)/ascorbate-induced peroxidation, as well as Fe(II)/ascorbate-induced lipid peroxidation in human colonic epithelial cells. PA at 100 μM and 500 μM effectively inhibited the decay of linoleic acid, both in the absence and presence of Fe(II)/ascorbate. The observed inhibitory effect of PA on Fe(II)/ascorbate-induced lipid peroxidation was lower (10–20%) compared to that of autoxidation. PA did not change linoleic acid hydroperoxides concentration levels after 24 hours of Fe(II)/ascorbate-induced peroxidation. In the absence of Fe(II)/ascorbate, PA at 100 μM and 500 μM significantly suppressed decomposition of linoleic acid hydroperoxides. Moreover, PA at the tested nontoxic concentrations (100 μM and 500 μM) significantly decreased 4-hydroxyalkenal levels in Caco-2 cells which structurally and functionally resemble the small intestinal epithelium. It is concluded that PA inhibits linoleic acid oxidation and reduces the formation of 4-hydroxyalkenals. Acting as an antioxidant it may help to prevent intestinal diseases induced by oxygen radicals and lipid peroxidation products.

In this study, we evaluated the usefulness of two commercially available hyaluronic acid-based hydrogels, HyStem and HyStem-C, for the cultivation of Wharton’s jelly mesenchymal stem cells (WJ-MSCs) and their differentiation towards chondrocytes. The WJ-MSCs were isolated from umbilical cord Wharton’s jelly using the explant method and their immunophenotype was evaluated via flow cytometry analysis. According to the criteria established by the International Society for Cellular Therapy, they were true MSCs. We assessed the ability of the WJ-MSCs and chondrocytes to grow in three-dimensional hydrogels and their metabolic activity. Chondrogenesis of WJ-MSCs in the hydrogels was determined using alcian blue and safranin O staining and real-time PCR evaluation of gene expression in the extracellular matrixes: collagen type I, II, III and aggrecan. Chondrocytes and WJ-MSCs cultured in the HyStem and HyStem-C hydrogels adopted spherical shapes, which are characteristic for encapsulated cells. The average viability of the WJ-MSCs and chondrocytes in the HyStem hydrogels was approximately 67 % when compared with the viability in 2D culture. Alcian blue and safranin O staining revealed intensive production of proteoglycans by the cells in the HyStem hydrogels. Increased expression of collagen type II and aggrecan in the WJ-MSCs cultured in the HyStem hydrogel in the presence of chondrogenic medium showed that under these conditions, the cells have a high capacity to differentiate towards chondrocytes. The relatively high viability of WJ-MSCs and chondrocytes in both HyStem hydrogels suggests the possibility of their use for chondrogenesis. The results indicate that WJ-MSCs have some degree of chondrogenic potential in HyStem and HyStem-C hydrogels, showing promise for the engineering of damaged articular cartilage.

To find better strategies to enhance the cytotoxic effect of paclitaxel (PTX) and lapatinib (LAP) against breast cancer cells, we analyzed the efficacy of a novel delivery system containing polylactide-co-poly(ethylene glycol) (PLA-PEG) filomicelles of over 100 nm in length and spherical micelles of approximately 20 nm in diameter. The ¹H NMR measurements confirmed the incorporation of PTX and LAP into micelles. Analysis of the drug release mechanism revealed the diffusion-controlled release of LAP and anomalous transport of PTX. Drug content analysis in lyophilized micelles and micellar solution showed their good storage stability for at least 6 weeks. Blank micelles, LAP-loaded micelles and free LAP did not affect MCF-7 breast cancer cell proliferation, suggesting that the cytotoxicity of PTX-, PTX/LAP-loaded micelles, and the binary mixture of free PTX and LAP was solely caused by PTX. PTX/LAP-loaded micelles showed greater toxicity compared to the binary mixture of PTX and LAP after 48 h and 72 h. Only free PTX alone induced P-gp activity. This study showed the feasibility of using a LAP and PTX combination to overcome MDR in MCF-7 cells, particularly when co-loaded into micelles. We suggest that PTX/LAP micelles can be applicable not only for the therapy of HER-2-positive, but also HER-2-negative breast cancers.