Background: Punicic Acid (PA) is a polyunsaturated fatty acid that accounts for approximately 70%- 80% of Pomegranate Seed Oil (PSO). PA possesses strong antioxidant, anti-inflammatory, anti-atherogenic effects, and anti-tumorigenic properties. Pomegranate extracts have been shown to have anticancer activity in many studies. However, there is no evidence for the effect of PSO on T98 glioblastoma cells. Therefore, the present study was the first to investigate the mechanisms induced by PA on T98 cells, which is one of the major compounds extracted from PSO. Methods: The effects of PA on cell viability; oxidative stress; and migration, proliferation, and apoptosis at the IC50 dose were studied. Results: The proliferation and migration were inhibited in the treated group compared to the non-treated group by 9.85µl/ml PA. The difference was statistically significant (***p<0.001). Furthermore, PA-induced apoptosis in the T98 glioblastoma cells compared to non-treated group and the difference was statistically significant (***p<0.001). Apoptosis was determined via immunocytochemistry staining of caspase-3, caspase-9 and TUNEL methods. Apoptosis was checked by flow cytometry (using caspase 3 methods) and Scanning Electron Microscopy Analysis. We also investigated the potential signaling pathway underlying this apoptotic effect. The immunocytochemical stainings of PI3K/ Akt-1/ mTOR-1 demonstrated that Akt-1 staining was increased with PA treatment similar to mTOR-1 and PI3K staining (***p<0.001). These increases were statistically significant compared to the non-treated group. Conclusion: PA exhibited exceptional abilities as an anticancer agent against GBM cells. The use of punicic acid in combination with other drugs used in the treatment of glioblastoma may increase the efficacy of the treatment. This study provided a basis for future investigation of its use in preclinical and clinical studies.

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OC has a protective effect on neural cells after TBI. This effect is achieved by reducing oxidative stress and apoptosis.

IntroductionStem cells exhibit self-renewal characteristics that distinguish them from other cell types. Major subtypes include totipotent cells, which can divide to produce all cells in an organism, pluripotent cells, which are able to differentiate into any of the three germ layers (endoderm, ectoderm, or mesoderm), and multipotent cells, which can produce multiple cell types within a given lineage (1). Mesenchymal stem cells (MSCs) constitute a class of multipotent cells capable of differentiating into many diverse cell types, including neural cells, chondroblasts, adipocytes, bone, skeletal muscle, and connective tissue (2-4). These cells can be isolated from almost any tissue, including bone marrow, Wharton jelly, umbilical cord, placenta, dental pulp, and adipose tissue using a simple procedure (5). Identification of MSCs is primarily performed using specific phenotypic and cell surface markers. MSCs should be able to adhere to a plastic surface and express defined surface antigens such as CD29, CD73, CD90, and CD105; however, they should also be negative Background/aim: Bone marrow-derived mesenchymal stem cells (BMSCs) possess self-renewal characteristics that distinguish them from other cell types. Recent studies have focused on the effects of conditioned medium (CM) that includes the extracellular matrix.Here we examined the neuroprotective effects of BMSCs and CM on damaged neuroblastoma cells. Materials and methods:The cells were divided into five groups: 1) healthy controls, 2) damaged cells alone, 3) damaged cells treated with BMSCs, 4) damaged cells treated with CM, and 5) damaged cells treated with both BMSCs and CM. Neuroprotective effects were then evaluated based upon the levels of oxidative stress, antitransforming growth factor β1 (anti-TGFβ1) production, and apoptosis.Results: Significant differences were observed between healthy controls and damaged cells (P < 0.001), as well as between damaged cells and those treated with BMSCs alone (P < 0.05), CM alone (P < 0.05), and both BMSCs and CM in combination (P < 0.01). Among the treated groups, the strongest neuroprotective effects were seen in cells treated with both BMSCs and CM. Conclusion:These results show that both BMSCs and CM exhibit neuroprotective effects in damaged neuroblastoma cells. The strongest benefits were seen following treatment with both BMSCs and CM.

The integrity of healthy skin plays a crucial role in maintaining physiological homeostasis of the human body. Chronic conditions such as diabetes mellitus or peripheral vascular diseases can lead to impaired wound healing. Skin wound healing purposes focusing on the main phases of wound healing, i.e., inflammation, proliferation, epithelialization, angiogenesis, remodeling, and scarring. This is a complex process, which is dependent on many cell types and mediators interacting in a highly sophisticated temporal sequence. Although some interactions during the healing process are crucial, redundancy is high and other cells or mediators can adopt functions or signaling without major complications. Mesenchymal stem cells have an alternative role due to special properties such as the capacity for self-renewal and multi-lineage differentiation, immunomodulatory effect, alleviation of inflammatory response, induction of angiogenesis, regulation of extracellular matrix remodeling, excellent migration and secretion of growth factors and cytokines in wound healing. We summarized current research on the mechanisms of mesenchymal stem cells with their isolation, specific markers, differentiation capacity, and the functional activities to evaluate wound healing application.