PubMed İndeksli Yayınlar Koleksiyonu
Permanent URI for this collectionhttps://hdl.handle.net/11727/4810
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Item Antiproliferative and Mitochondrial Protective Effects of Apigenin in an Oxygen-Induced Retinopathy In Vivo Mouse Model(2021) Sezenoz, Almila Sarigul; Akkoyun, Imren; Helvacioglu, Fatma; Haberal, Nihan; Dagdeviren, Attila; Bacanli, Didem; Yilmaz, Gursel; Oto, Sibel; 0000-0002-2860-7424; 34665015; AAK-7713-2021Purpose: To investigate the effects of a common dietary flavonoid apigenin on retinal endothelial cell proliferation, retinal morphological structure, and apoptotic cell death in an oxygen-induced retinopathy (OIR) mouse model to evaluate the possibility of the use of apigenin in the treatment of ocular neovascular diseases (ONDs). Methods: Ninety-six newborn C57BL/6J mice were included. Eight groups were randomized, each including 12 mice. Two negative control groups were kept in room air: the first without any injection and the second received intravitreal (IV) dimethyl sulfoxide (DMSO), which is the solvent we used. The OIR groups were exposed to 75% +/- 2% oxygen from postnatal days (PD) 7 to 12. On PD 12, the mice were randomly assigned to 6 groups: 2 OIR control groups (1 received no injection, 1 received IV-DMSO), 2 IV-apigenin groups (10 and 20 mu g/mL), and 2 intraperitoneal (IP)-apigenin groups (10 and 20 mg/kg). We quantified retinal endothelial cell proliferation by counting neovascular tufts in cross-sections and examined histological and ultrastructural changes through light and electron microscopy. We evaluated apoptosis by terminal deoxynucleotidyl transferase-mediated nick end-labeling (TUNEL). Results: We detected a significant increase in endothelial cell proliferation in the OIR groups. Groups receiving apigenin, both IP and IV, had significant decreases in endothelial cells, atypical mitochondrion count, and apoptotic cells compared with the groups receiving no injections. None of the apigenin-injected groups revealed cystic degeneration or cell loss. Conclusions: Apigenin suppresses neovascularization, has antiapoptotic and antioxidative effects in an OIR mouse model, and can be considered a promising agent for treating OND. Clinical trial (Project number: DA15/19).Item Effect of Creatine on Rat Sciatic Nerve Injury: A Comparative Ultrastructural Study(2018) Helvacioglu, Fatma; Kandemir, Ersin; Karabacak, Busra; Karatas, Idil; Pecen, Ahmet; Ercan, Ipek; Sencelikel, Tugce; Dagdeviren, Attila; 0000-0002-6048-3951; 0000-0002-6026-0045; 0000-0001-8990-8282; 27858383; AAI-6791-2021; AAH-8887-2021; P-2877-2014AIM: Creatine is an endogenous molecule synthesized in the liver, kidney and pancreas from glycine and arginine and is important for mitochondrial metabolism. It is widely used as a supplement for improving muscle mass and function for many years. As it is expected to prevent apoptosis and diminish oxidative stress, it is also studied in a number of neurodegenerative diseases for its beneficial effect in recent years. We studied the effect of creatine on the peripheral nerve injury in an experimental rat crush injury model to obtain ultrastructural evidence. MATERIAL and METHODS: Animals were randomly divided into 3 groups having 5 animals in each group. Group 1 was the control group, Group 2 the trauma group and Group 3 the trauma+ creatine group. The first group served as sham control. In group 2 and group 3, sciatic nerves of the rats received crush injury using aneurysm clips. In group 3, daily 2 g/kg creatine monohydrate was administered via gavage after the trauma. Nerve samples were obtained at the 28th day after trauma for light and electron microscopic evaluation. RESULTS: Our comparative analysis results suggest a possible positive effect of creatine supplement on peripheral nerve regeneration as statistical analysis revealed significant differences between group 2 and group 3. Though our finding does not represent a miracle of regenerative support, beneficial usage of creatine is documented in the present study. CONCLUSION: Creatine supplement helps to diminish the harmful effects of peripheral nerve crush injury which is also supported by electron microscopy findings.