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| 1 | Melatonin reduces traumatic brain injury-induced oxidative stress in the cerebral cortex and blood of rats显示文摘Free radicals induced by traumatic brain injury have deleterious effects on the function and antioxidant vitamin levels of several organ systems including the brain. Melatonin possesses antioxidant effect on the brain by maintaining antioxidant enzyme and vitamin levels. We investigated the effects of melatonin on antioxidant ability in the cerebral cortex and blood of traumatic brain injury rats. Results showed that the cerebral cortex β-carotene, vitamin C, vitamin E, reduced glutathione, and erythrocyte reduced glutathione levels, and plasma vitamin C level were decreased by traumatic brain injury whereas they were increased following melatonin treatment. In conclusion, melatonin seems to have protective effects on traumatic brain injury-induced cerebral cortex and blood toxicity by inhibiting free radical formation and supporting antioxidant vitamin redox system. | Nilgün Senol Mustafa Naziroglu | 2014 | Neural Regeneration Research2014，9，11： | 5 |
| 2 | Moderate exercise combined with dietary vitamins C and E counteracts oxidative stress in the kidney and lens of streptozotocin -induced diabetic rat 显示文摘 | KUTLU Mehmet NAZIROGLU Mustafa SIMSEK Halil | 2005 | International journal for vitamin and nutrition research2005，75，： | 1 |
| 3 | Levels of lipid peroxidation and antioxidant vitamins in plasma and erythroeytes of patients with ankylosing spondylitis 显示文摘 | Naziroglu Mustafa Akkus | 2011 | Clin Biochem2011，44，17： | 1 |
| 4 | Modulation of oxidative stress, apoptosis, and calcium entry in leukocytes of patients with multiple sclerosis by Hypericum perforatum显示文摘 | Yurekli Mustafa Naziroglu Suleyman | 2014 | Nutritional neuro-science2014，17，5： | 1 |
| 5 | Protective effects of nanostructures of hydrated C 60 fullerene on reproductive function in streptozotocin-diabetic male rats显示文摘 | Ramazan Bal Gaffari Türk Mehmet Tuzcu Okkes Yilmaz Ibrahim Ozercan Tuncay Kuloglu Seyfettin Gür Victor S. Nedzvetsky Artem A. Tykhomyrov Grigory V. Andrievsky Giyasettin Baydas Mustafa Naziroglu | 2010 | Toxicology2010，，3： | 1 |
| 6 | Effects of astaxanthin on antioxidant parameters in ARPE-19 cells on oxidative stress model显示文摘AIM: To observe the protective effect of astaxanthin(AST) against hydroquinone(HQ) mediated cell death in the apoptotic cascade and evaluate intracellular Ca2+ release, caspase-3, and-9 activation, reactive oxygen species(ROS) production in ARPE-19 cells.METHODS: We cultured ARPE-19 cells in special mediums and performed MTT tests to determine protective effect of AST, before exposing the cells to HQ in an incubator. We analyzed intracellular Ca2+ release experiments, mitochondrial membrane depolarization, glutathione(GSH), glutathione peroxidase(GSH-Px) and ROS experiments, and apoptosis assay.RESULTS: ROS production ranges depend on the amount of cell death. We computed the correlation between ROS ranges and cell death by 20,70-dichlorofluorescein fluorescence, and Ca2+ levels by Fura-2-AM. HQ-induced cell death found out to rise ranges of caspase-3 and-9, and mitochondrial depolarization. These three steps were delayed by AST management.CONCLUSION: ARPE-19 cells are avoided from HQinduced ROS production and caspase-3 and-9 activation by AST. AST may limit the range of caspase synthesis, Ca2+ release and excess production of ROS with antiapoptotic effect. This study proposes a new therapeutic approach for the treatment of age-related macular degeneration. | Yigit Musa Günes Alime Uguz Cihangir Yalcin Tok Ozlem Tok Levent Oz Ahmi Naziroglu Mustafa | 2019 | International Journal of Ophthalmology(English edition)2019，12，6： | 1 |
| 7 | An extract of Hypericum perforatum induces wound healing through inhibitions of Ca^(2+) mobilizations,mitochondrial oxidative stress and cell death in epithelial cells:Involvement of TRPM2 channels显示文摘The wound is induced by several mechanical and metabolic factors.In the etiology of the wound recovery,excessive oxidative stress,calcium ion(Ca^(2+))influx,and apoptosis have important roles.Ca^(2+)-permeable TRPM2 channel is activated by oxidative stress.Protective roles of Hypericum perforatum extract(HP)on the mechanical nerve injury-induced apoptosis and oxidative toxicity through regulation of TRPM2 in the experimental animals were recently reported.The potential protective roles in HP treatment were evaluated on the TRPM2-mediated cellular oxidative toxicity in the renal epithelium(MPK)cells.The cells were divided into three groups as control,wound,and wound+HP treatment(75μM for 72 h).Wound diameters were more importantly decreased in the wound+HP group than in the wound group.In addition,the results of laser confocal microscopy analyses indicated protective roles of HP and TRPM2 antagonists(N-(p-Amylcinnamoyl)anthranilic acid and 2-aminoethyl diphenylborinate)against the wound-induced increase of Ca^(2+) influx and mitochondrial ROS production.The wound-induced increase of early(annexin V-FITC)apoptosis and late(propidium iodide)apoptosis were also decreased in the cells by the HP treatment.In conclusion,HP treatment acted protective effects against wound-mediated oxidative cell toxicity and apoptosis through TRPM2 inhibition.These effects may be attributed to their potent antioxidant effect. | FUAT USLUSOY MUSTAFA NAZIROGLU | 2019 | BIOCELL2019，43，4： | 0 |
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