50 research outputs found

    Growth Factors Responsible from the Cancer Progress: Role of Natural Products

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    Growth factors are one of the main factors responsible from the uncontrolled cell progress in cancer. Up to date many scientists have focused on these factors either as the marker or as the targets in several cancer types. Mainly the drugs are designed to target these factors are monoclonal antibodies. Nerve growth factor (NGF), epidermal growth factor (EGF), hepatocyte growth factors (HGF), fibroblast growth factors (FGF), vascular endothelial growth factors (VEGF), platelet derived growth factor (PDGF), transforming growth factor (TGF-β) are some of these factors not only increasing the ability of cell proliferation but also playing crucial roles in triggering the invasion and metastasis of the cells. The herbs that are traditionally used for anticancer treatment and target multiple interdependent processes. Given the multiple effects of these agents, their future use for cancer therapy probably lies in synergistic combinations. For instance, Artemisia annua, Viscum album, Curcuma longa, Camellia sinensis, Vitis vinifera, Angelica sinensis, Taxus brevifolia, are some of the herbs that has shown to affect VEGF and those which have additional effects on the molecules related to cancer progress and further can target other growth factors. During active cancer therapy, they should generally be evaluated in combination with chemotherapy and radiation. In this role, they act as modifiers of biologic response, potentially enhancing the efficacy of or reducing the resistance to the conventional therapies

    The Effects of Aldose Reductase Inhibitor Quercetin and Monochloropivaloylquercetin in Amyloid beta Peptide (1-42) Induced Neuroinflammation in Microglial Cells

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    Microglial over-activation plays a crucial roles during neuroinflammation. Aldose reductase (AR) is one of the enzymes that has been linked to inflammatory processes in several diseases. Therefore, inhibition of AR is considered as an important strategy to reduce inflammation. In the present study, Quercetin (Q) and monochloropivaloylquercetin (MCPQ) showed potent inhibition on AR expression and anti-neuroinflammatory effects in Amyloid beta (A beta) peptide (1-42) induced inflammatory process by inhibiting expression of inflammatory mediators from microglial cells. Furthermore, ablation of AR caused a significant reduction on COX2 expression in A beta-induced neuroinflammation. Q and MCPQ suppressed COX2 mRNA and protein expression, which further resulted in downstream inhibition of prostaglandin E-2 (PGE(2)) release in A beta-induced neuroinflammatory process. Additionally, All treatment resulted in activation of Mitogen Activated Protein Kinase (MAPK) and increased translocation of Nuclear Factor Kappa B (NF kappa B). Q and Sorbinil significantly reduced the activation of MAPK, at the same time Q, MCPQ and sorbinil decreased nuclear translocation of NF kappa B and diminished tumor necrosis factor (TNF)-alpha release in A beta-induced neuroinflammation. The results suggested that AR is a probable target for treatment of neuroinflammation as well as Q and MCPQ could be effective agents for treating or preventing inflammation-related neurodegenerative diseases by AR inhibition

    The importance of circadan rhythm alterations in erythrocyte deformability

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    The hormone melatonin, secreted from the pineal gland at night and suppressed during the day, provides a circadian and seasonal signal to the organism. The impact of pharmacological doses of melatonin on erythrocyte deformability was investigated by our group in several studies in both in vitro and in vivo conditions. The aim of this study was to investigate the effects of alterations in the physiological melatonin levels via the circadian rhythm on erythrocyte deformability. 50 male rats weighing 250-300 g were divided in 5 groups. The rats were subjected to 12/12, 24/0, 0/24, 16/8 and 8/16 h of Light/Dark (L/D) cycle, respectively. The elongation indexes (EI) of the erythrocytes were measured by a laser diffractometer (Myrenne Rheodyne SSD) by using 30 mu l of whole blood suspended in 2 ml of Dextran 60. There was no significant difference in the EI of the 24/0 h L/D group compared to the control (12/12), whereas the decrease of EI was statistically important in the 0/24 h L/D group (p=0.009). This decrease in EI was also significant when this group was compared to the 24/0 h L/D group (p=0.05). Furthermore, the EI was affected significantly by alterations in the circadian rhythm, compared to control (16/8, 8/16 h L/D; p=0.05 and p=0.007, respectively). As a result, the alterations in physiological melatonin levels via different circadian rhythms have significant impacts on the deformability of erythrocytes, which therefore may cause important cardiovascular implications in the people who are exposed to different light dark cycles. Furthermore, these data represents a new and a quite crucial open-field to be investigated and taken into account in in vivo hemorheological studies

    alpha-Chaconine and alpha-Solanine Inhibit RL95-2 Endometrium Cancer Cell Proliferation by Reducing Expression of Akt (Ser473) and ER alpha (Ser167)

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    The aim of this study is to investigate the potential inhibitory effect of alpha-chaconine and alpha-solanine on RL95-2 estrogen receptor (ER) positive human endometrial cancer cell line and to identify the effect of these glycoalkaloids on the Akt signaling and ER alpha. The cell proliferation profiles and the cytotoxicity studies were performed by Real-Time Cell Analyzer (xCELLigence) and compared with Sulphorhodamine B (SRB) assay. The effects of alpha-chaconine (2.5, 5, 10 mu M), alpha-solanine (20, 30, 50 mu M), API-1 (25 mu M) and MPP (20 mu M) effects on Akt (Ser473) and ER alpha (Ser167) expressions evaluated by Western blot and qPCR method. Their IC50 values were as alpha-chaconine (4.72 mu M) < MPP (20.01 mu M) < alpha-solanine (26.27 mu M) < API-1 (56.67 mu M). 10 mu M alpha-chaconine and 20, 30 and 50 mu M alpha-solanine were effective in decreasing p-Akt(Ser473)/Akt ratio compared to positive control API-1. When the p-ER alpha/ER alpha ratios were evaluated, it was observed that alpha-chaconine (2.5, 5, 10 mu M) and alpha-solanine (50 mu M) were as effective as the specific ER alpha inhibitor MPP in reducing the ratio of p-ER alpha/ER alpha compared to the control group. In conclusion, it has been shown that the proliferation of alpha-chaconine and alpha-solanine in human endometrial carcinoma cells reduces the expression and activity of the Akt and ER alpha signaling pathway

    The Effects of α-Chaconine on ER-α Positive Endometrium Cancer Cells

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    Endometrial cancer is one of the most common cancer types among women in the world. In our study, it was aimed to investigate the potential anticancer effect of α-chaconine, which is one of the major glycoalkaloids found in Solanum tuberosum (potato), on estrogen receptor (ER) positive endometrial cancer cell line RL95-2. The effect of α-chaconine on RL95-2 cell viability was determined by the method of sulforhodamine B. Effect of α-chaconine on cell growth curve was assessed with the real-time cell analyzer system (xcelligence). The ERα inhibitor methyl-piperidino-pyrazole (MPP) dihydrochloride was used as a positive control to evaluate the association of α-chaconine with ERα. Expressions of ERα and p-ERα protein level were investigated by western blot. ERα mRNA expressions were performed by the real-time PCR method. The IC50 values ​​ of MPP dihydrochloride and α-chaconine were calculated as 20.01 μM and 4.72 μM, respectively. At MPP dihydrochloride 20 μM (p &lt; 0.001), α-chaconine; 2.5 (p &lt; 0.001); 5 (p &lt; 0.001) and 10 μM (p &lt; 0.001) concentrations, p-ERα/ERα ratio was decreased in the same significance compared to control. α-Chaconine decreased the level of ERα mRNA expression, after 24 h, but this decrease was not significant. This study showed for the first time the effect of α-chaconine on cell proliferation, ERα activity and expression in RL95-2 cells

    The availability of vocal training for improvement of accent and articulation defects in speech education

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    This study is designed to test the use of vocal training for articulation and accent defects which might be an important trouble while Turkish speaking. For this reason vocal training has been performed on a group of students selected voluntarily form the Erciyes University Turkish teaching profession 3rd class and the difference before and after vocal training accent and articulation defect improvements have been evaluated. To reach this general purpose pre-test and pro-test applications have been tested by "Vitalograph Alpha, Model 6000" portable spirometer device and "Praat vocal analyze program". Breathe management and thereby the accent factors that effect speaking are evaluated on even if they were improved after a programmed vocal training study over VC, FVC and FEV1 parameters. After voice training FVC (p<0.001) decreased and FEV1 (p<0.001) increased significantly whereas the VC has not changed significantly. Furthermore, with the help of the data obtained from the Praat vocal analyze program the accent and articulation defects have been evaluated over "Turk" and "vazifen" words and the duration of the voice the intensity, amplitude, maximum power frequency and pitch values are analyzed. This analyze revealed that after vocal training when we consider the "Turk" word, the intensity (p<0.05), amplitude (p<0.05), harmonics to noise ratio (p<0.05), duration (p<0.001) increased significantly. When we consider the word "vazifen", the intensity (p<0.05), amplitude (p<0.001), harmonics to noise ratio (p<0.001) and duration (p<0.001) increased significantly, the pitch significantly decreased (p<0.001). In conclusion, in the students who are having Turkish speaking education, vocal training studies are seen to be useful to improve the articulation and accent defects, which means that it is helpful to state accent expressions and breathe management to express the Turkish words correctly. (C) 2012 Published by Elsevier Ltd. Selection and/or peer review under responsibility of Prof. Dr. Huseyin Uzunboyl

    Detection of natural compounds by virtual screening, molecular docking and dynamics studies and evaluation of their effects on tau level in vitro Alzheimer's model.

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    In Alzheimer’s disease (AD), neurofibrillary tangles are composed of hyperphosphorylated tau protein, and tau hyperphosphorylation reduces microtubule binding. Many protein kinases are thought to be involved in tau hyperphosphorylation. Based on the fact that tau hyperphosphorylation can be prevented by inhibition of glycogen synthase kinase-3β (GSK-3β), which is one of the tau kinases, the effectiveness of potential GSK-3β inhibitors determined by virtual screening, molecular docking, and dynamics simulations studies on Alzheimer’s pathology has been examined and its role in neurodegeneration has been investigated by studies. Neomangiferin was determined as the most effective molecule according to the results of studies with potential compounds determined by virtual screening and molecular docking to be GSK-3β inhibitors in the in vitro Alzheimer’s model created by neuronal differentiation studies. Neomangiferin has been shown to have a protective role in induced neurodegeneration by the MTT method and Real Time Cell Analysis. It has been determined that Neomangiferin inhibits GSK-3β and reduces the level of phosphorylated tau. In summary, our findings suggested Neomangiferin can be a therapeutic candidate for AD treatment. Communicated by Ramaswamy H. Sarma
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