Investigation of UV-treated mesenchymal stem cells in an in vitro wound model.

This study examines the effects of ultraviolet-induced adipose tissue-derived mesenchymal stem cells and their supernatants on wound healing regarding cell viability, percentage of wound healing, released cytokine, and growth factors. It has been reported in previous studies that mesenchymal stem cells are resistant to ultraviolet light and have a protective effect on skin cells against ultraviolet-induced damage. At the same time, there are many studies in the literature about the positive effects of cytokines and growth factors secreted by mesenchymal stem cells. Based on this information, the effects of ultraviolet-induced adipose-derived stem cells and supernatants containing their secreted cytokines and growth factors on an in vitro two-dimensional wound model created with two different cell lines were investigated in this study. It was determined from the results that the highest cell viability and the least apoptotic staining were 100 mJ in mesenchymal stem cells (**p < 0.01). Furthermore, analysis of cytokines and growth factors collected from supernatants also supported 100 mJ as the optimal ultraviolet dose. It was observed that cells treated with ultraviolet and their supernatants significantly increased cell viability and wound-healing rate over time compared to other groups. In conclusion, with this study, it has been shown that adipose-derived stem cells exposed to ultraviolet light can have an important use in wound healing, both with their potential and with the more cytokines and growth factors they secrete. However, further analysis and animal experiments should be performed before clinical use.

Comparison of the different isoforms of vitamin e against amyloid beta-induced neurodegeneration.

Neurodegeneration is the progressive loss of structure or function of neurons. Amyloid beta oligomers and aggregates have been linked to neurodegeneration. While previous studies have suggested that dietary α-tocopherol intake can prevent amyloid beta aggregation and protect the brain against neurotoxicity, other research, however, indicated that tocotrienol forms might be used as an alternate agent against this kind of degeneration. In the presented research, we compared the in vitro protective effects of α-tocopherol and α-tocotrienol. In this context, we formed an in vitro neurodegeneration model with primary isolated neurons and measured α-tocopherol's and α-tocotrienol's protective effects. As a result, α-tocopherol and α-tocotrienol prevent the degeneration of neurons. Moreover, α-tocopherol and α-tocotrienol regulated the neuron's calcium channels mechanism by decreasing the expression of the calcium channel alpha 1C subunit. We also observed that the amount of amyloid beta accumulation in the extracellular matrix decreased with the application of these isoforms. In specific time points, α-tocopherol and α-tocotrienol differ in terms of protective effects. In conclusion, it could be interpreted that, in more extended periods, α-tocotrienol could be a significant protective agent against amyloid beta-induced neurodegeneration, and it can be used as an alternative to other protective agents, especially α-tocopherol.