The effect of Korean red ginseng on mesenchymal stem cells from healthy and osteoporotic human bone marrow.

BACKGROUND: Osteoporosis is a disease characterized by an increase in bone fragility as a result of decreased bone mass and weakening of the bone structure. There are studies on the relationship between osteoporosis and hearing and balance system. The goal of this study was to compare the proliferation and osteogenesis induction properties of mesenchymal stem cells derived from healthy and osteoporotic individuals to better understand the healing properties of Korean red ginseng (KRG) and Panax ginseng-Avena Sativa-Tribulus Terrestris mixture (PAT). MATERIALS AND METHODS: Osteoporotic and healthy MSCs were isolated successfully in culture conditions. The proliferation levels of cells treated with different doses of KRG and PAT were compared by Water-Soluble Tetrazolium-1 (WST-1) assay. Alkaline phosphatase (ALP) assay was performed by selecting the most effective KRG dose in proliferation. RESULTS: Morphology of isolated cells and the expression of cell surface antigens have been detected as similar. The WST-1 assay showed that KRG was effective on the proliferation of osteoporotic cells. The levels of ALP in osteoporotic cells treated with KRG is increased depending on the differentiation day compared to healthy cells. CONCLUSION: KRG triggered an increase in intracellular ALP levels of osteoporotic MSCs. It suggests that KRG on osteoporotic cells is influential in stimulating osteogenesis and may be useful in osteoporotic patients.

Glioblastoma Stem Cells and Comparison of Isolation Methods.

BACKGROUND: Glioblastoma (GBM) is the most aggressive and the most common primary brain tumor. Over the last few years, studies have identified many genetical and phenotypical molecular situations for developing new treatment modalities in patients with GBM. Nevertheless, main problem for the GBM is radio-chemotherapy resistance and relapse after the surgery. The identification of glioma stem cells and microenvironmental influences has created a paradigm shift in targets of therapy. Current studies have shown that glioma stem cell is responsible for aggressiveness, recurrence and resistance to therapy of GBM. GBM stem cell isolated from human GBM multiforme fresh tissue samples is important both for curative therapeutic options and personalized targeted therapy. The purpose of this study was to determine the most suitable isolation method of GBM stem cells (GSCs). METHODS: Tumor tissue sample was obtained during the surgical resection of lesion in patients with the diagnosis of GBM. Tumor stem cell isolation from tissue was performed in three different ways: 1) GBM cell isolation with trypsin; 2) GBM cell isolation with brain tumor dissociation Kit (BTD Kit); and 3) GBM cell isolation with tumor dissociation enzyme (TDE). RESULTS: We showed that GSCs were isolated from tumor specimen using flow cytometry and immunofluorescence staining. Our study showed that isolation with BTD Kit is the most suitable method to isolate GBM tissue-derived glial tumor stem cells. CONCLUSIONS: The development of alternative personalized therapies targeting brain tumor stem cell is urgently needed. It is important to understand the fundamental mechanisms of driving stem cells. If their life cycle mechanisms can be identified, we can control the growth of GBM.

Diclofenac induced apoptosis via altering PI3K/Akt/MAPK signaling axis in HCT 116 more efficiently compared to SW480 colon cancer cells.

Diclofenac is a preferential cyclooxygenase 2 inhibitor (COX-2) and member of non-steroidal anti-inflammatory drugs (NSAIDs). Inflammation is one of the main reason of poor prognosis of colon cancer cases; thereby NSAIDs are potential therapeutic agents in colon cancer therapy. In this study, our aim to understand the potential molecular targets of diclofenac, which may propose new therapeutic targets in HCT 116 (wt p53) and SW480 (mutant p53R273H) colon cancer cells. For this purpose, we identified different response against diclofenac treatment through expression profiles of PI3K/Akt/MAPK signaling axis. Our hypothesis was diclofenac-mediated apoptosis is associated with inhibition of PI3K/Akt/MAPK signaling axis. We found that sub-cytotoxic concentration of diclofenac (400 µM) promoted further apoptosis in HCT 116 cells compared to SW480 colon cancer cells. Diclofenac triggered dephosphorylation of PTEN, PDK, Akt, which led to inhibition of PI3K/Akt survival axis in HCT 116 colon cancer cells. However, diclofenac showed lesser effect in SW480 colon cancer cells. In addition, diclofenac further activated p44/42, p38 and SAPK/JNK in HCT 116 cells compared to SW480 cells.