International Journal of Medical Laboratory

Background and Aims: Metabolic syndrome, a common metabolic disorder, for the serious health consequences such as insulin resistance and lipid abnormalities has been considered as a major clinical challenge with obscure causes. Oxidative stress is an important component of metabolic syndrome, contributing in its development. Troxerutin, a semi-synthetic derivative of natural bioflavonoid rutin, exerts various pharmacological activities, which among all, strong anti-oxidative property is of great importance. The aim of the current study was to evaluate the effects of troxerutin on metabolic parameters and oxidative stress in metabolic syndrome induced by fructose in male rats.
Materials and Methods: In order to induce metabolic syndrome, animals received the water containing 20% fructose for 8 weeks. Troxerutin was administered to animals with the dose of 150 mg/kg orally for 4 weeks after induction of metabolic syndrome following biochemical analysis and oxidative stress marker assessment.
Results: Data showed that high-fructose diet leads to elevation of blood glucose and insulin resistance and causes abnormalities in lipid profile as well as oxidative stress enhancement (signs of a metabolic syndrome) (p<0.001). Troxerutin administration improved the detrimental effects of metabolic syndrome on biochemical factors and diminished oxidative stress (p<0.001).
Conclusions: Troxerutin administration reverses the deleterious effect of metabolic syndrome in rats with high-fructose diet.

Background and Aims: Previous studies have shown that adipose-derived mesenchymal stem/ stromal cells are one of the sources of mesenchymal stem cells (MSCs) with the capacity to differentiate into various mesodermal cell lineages. MSCs with cytokines secretion capability, which contributes to repair damaged tissues have gained wide credence for future cell-based therapeutic applications. In this study, the effect of the different dosages of vitamin E and Selenium was assessed on the stemness of the human adipose tissue-derived MSCs (AD-MSCs).
Materials and Methods: Following 24 hours of cell treatments with different dosages of vitamin E and Selenium, MTT assay was used to assess the effect of them on cell proliferation. Moreover, the stemness of the AD-MSCs was assessed using osteogenic and adipogenic induction medium supplemented with the different dosages of the vitamin E and Selenium. Finally, Alizarin red and Oil-red O staining were performed to detect matrix mineralization and lipid droplet accumulation, respectively.
Results: MTT data revealed that the optimal concentration for vitamin E and Selenium were 125 µM and 121 µM for the viability of the AD-MSCs. Moreover, the effect of vitamin E and Selenium were assessed by osteogenic and adipogenic differentiation by optimal dosages obtained by MTT assay, respectively. Maximum mineralization and lipid droplet aggregation of the differentiated cells were detected at IC50 in comparison with the control group.
Conclusions: These results suggest that different dosages of vitamin E and Selenium could have various impacts on the proliferation and differentiation induction of human AD-MSCs.

Background and Aims: It has been proven that human mesenchymal stem cells (MSCs) conditioned medium (hMSCs-CM) can influence human embryonic stem cells (hESCs) chondrogenic differentiation. In this study, we hypothesized that conditioned medium (CM) from hESCs-derived MSCs in a sequential 3D-2D culture system could facilitate the induction of chondrogenesis in hESCs.
Materials and Methods: CM was collected from Yazd2 (hESCs; 46, XY) derived MSCs confluent cultures and stored at -20 °C. Yazd4 hESC line (46, XX) was induced for differentiation using EB formation as 3D culture into SD (spontaneously differentiation) and CM groups (differentiation using conditioned medium) for four days. Cell culture continued in a 2D (monolayer) culture system for both groups till day 14. Ultimately, chondrogenic differentiation was assessed by Alcian blue and masson′s trichrome staining at 4 and 14 days of differentiation, and quantitative real-time polymerase chain reaction (PCR) for NANOG, MEOX1, SOX5, SOX6, SOX9, ACAN, COL2A1 and RUNX2 genes for SD and CM groups on days 0 and 4.
Results:  The gene expression profile for chondrogenic genes in the CM group was significantly more than the SD group (p< 0.05). Furthermore, chemical staining assessment illustrated a significant GAG and collagen II difference between the CM and SD groups at days 4 and 14 (p< 0.05).
Conclusions: Our findings would pave the way for creating an in vitro human chondrogenesis model for further studies in the developmental biology of articular cartilage tissue, which lend itself to cell-based therapy to cure joint diseases such as osteoarthritis.