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Öğe A possible protective role of betain and omega-3 supplementation in traumatic brain injury(Edizioni Luigi Pozzi, 2019) Ataizi, Serdar; Özkoç, Mete; Kanbak, Güngör; Karimkhani, Hadi; Burukoğlu Dönmez, Dilek; Üstünışık, Növber; Öztürk, BuketINTRODUCTION: Due to irreversible damage following head trauma, many overlapping pathophysiological events occur including excitotoxicity, acidotoxicity, ionic imbalance, edema, oxidative stress inflammation and apoptosis. MATERIAL AND METHODS: In this this study, after the rats were separated in to groups theserats were fed throughout fourteen days with betaine, omega-3 or betaine+omega-3 combination in physiological limits prior to the trauma. After a closed head trauma, the damaged brain tissues were collected for biochemically and histologically analyses. This examination involved analyses of levels of caspase-3 and cytochrome C and neuron-specific enolase (NSE) levels in brain tissue. RESULTS: These analyses showed that traumatic brain injury (TBI) caused an increase in the levels of caspase-3, cytochrome C and neuron-specific enolase (NED) in the brain tissues examined. DISCUSSION: In this study, apoptotic and/or necrotic cell death via mitochondrial cytochrome C caspase pathway in traumatized cells and neuron-specific enolase (NED) increase indicative of neuronal damage confirmed the research hypothesis. CONCLUSION: Level of the biomarkers induced by brain injury in the groups fed with betaine, omega-3 and betaine+omega-3 combination before the traumatic damage approximated to that of control group values, suggesting that these products may have a neuroprotective role.Öğe Dose-dependent effects of vitamin 1,25(OH)2D3 on oxidative stress and apoptosis(Walter de Gruyter GmbH, 2018) Çakıcı, Çağrı; Yiğitbaşı, Türkan; Ayla, Şule; Karimkhani, Hadi; Bayramoğlu, Feyza; Yiğit, Pakize; Kılıç, Ertuğrul; Emekli, NesrinThe purpose of this study is to examine the dose-dependent effects of vitamin 1,25(OH)2D3 on apoptosis and oxidative stress. In this study, 50 male Balb/c mice were used as control and experiment groups. The mice were divided into 5 groups each consisting of 10 mice. Calcitriol was intraperitoneally administered as low dose, medium dose, medium-high dose and high dose Vitamin D groups (at 0.5, 1, 5 and 10 µg/kg, respectively), for three times a week during 14 days. At the end of the study, annexin V was measured by enzyme-linked immunosorbent assay method, and total antioxidant capacity and total oxidant status values were measured by colorimetric method in serum. Hematoxylin eosin staining was performed in liver tissues and periodic acid schiff staining was performed in kidney tissues. While comparing the results of medium-high dose (5 µg/kg) and high dose (10 µg/kg) Vitamin D administration to that of the control group, it was observed that serum antioxidant status and annexin V levels decreased and glomerular mesenchial matrix ratio increased in kidney (p<0.05). In addition to these findings, in the group receiving high dose Vitamin D (10 µg/kg), it was observed that the damage to the liver increased together with the the oxidative stress index values (p<0.05). As a result, this study was the first in the literature to report that use of high-dose Vitamin D (10 µg/kg) results in oxidant effect, rather than being an antioxidant, and causes severe histopathological toxicity in the liver and kidney.Öğe Evaluation of the neuroprotective role of boric acid in preventing traumatic brain injury-mediated oxidative stress(Turkish Neurosurgical Society, 2021) Ataizi, Zeki Serdar; Özkoç, Mete; Kanbak, Güngör; Karimkhani, Hadi; Burukoğlu Dönmez, Dilek; Üstünışık, Növber; Öztürk, BuketAIM: To investigate the possible neuroprotective effect of boric acid (BA) by examining the changes in catalase (CAT) activity and levels of CAT and malondialdehyde (MDA) in brain tissues from rats with closed head trauma. MATERIAL and METHODS: The study consisted of three groups: control, traumatic brain injury (TBI) and TBI + BA. Animals in the control and TBI groups received saline, while animals in the TBI + BA group received BA through daily oral gavage, for 14 days prior to TBI was performed using the modified Marmarou impact acceleration model. After 24 hours, animals were euthanized, and brain tissue obtained to measure the levels of MDA and to assess the activity of CAT. RESULTS: MDA levels and CAT activity were significantly higher in the TBI group versus the control group. However, they were significantly lower in the TBI + BA group compared to TBI alone. Similarly, edema and necrotic neurons were observed in the TBI group, but not in the control or TBI + BA groups. CONCLUSION: Based on biochemical and histopathological evidence, we determined that TBI induced lipid peroxidation and oxidative stress were inhibited by pre-treatment with BA.Öğe Investigation of the protective effect of boric acid and omega-3 fatty acid in model of acute myocardial infarction changes in myocardial rats(Wiley-Blackwell, 2016) Karimkhani, Hadi; Özkoç, Mete; Kanbak, Güngör; Uzuner, Kubilay; Burukoğlu, Dilek[Abstract Not Available]Öğe Possible protective effects of betaine on liver and kidney tissues of long term therapeutic doses of paracetamol (acetaminophen) administered on pregnant rat's newborn puppies(Wiley-Blackwell, 2016) Özkoç, Mete; Karimkhani, Hadi; Kanbak, Güngör; Burukoğlu Dönmez, Dilek[Abstract Not Available]Öğe Protective effect of betaine against skeleton muscle apoptosis in rats induced by chronic alcohol and statin consumption(Comenius University, 2020) Oğlakçı İlhan, Ayşegül; Özkoç, Mustafa Furkan; Kuşat Ol, Kevser; Karimkhani, Hadi; Şentürk, Hakan; Burukoğlu, Dilek; Kanbak, GüngörAIM: The aim of the present study was to investigate the effect of apoptosis on rat skeletal muscle caused by chronic alcohol and statin consumption with modified liquid diet and to elucidate protective effects of betaine supplementation.METHODS: TNF-alpha (tumor necrosis factor), NF-kappa B (Nuclear Factor kappa B), cytochrome c and caspase-3 levels with or without betaine treatment in alcohol and/or statin-induced skeleton muscle apoptosis rats as well as in controls were measured in serum and tissue. Histologic examinations of the muscle tissues were also performed.RESULTS: In our study, betaine treated treatment groups we found that calpain and caspase activities and cytokine c release were decreased caused by alcohol, statin and more importantly alcohol+statin group and TNF and NF-kappa B levels were also close to the levels of control group. Similarly, significant improvements have been observed in our morphological and histological examination results also supporting our biochemical data.CONCLUSION: We found that combined consumption of ethanol and statin is capable of triggering apoptotic cell death in rat muscles more than the consumption of only alcohol or only statin. Betaine was able to reduced this muscle cell death induced by alcohol and/or statin consumption.Öğe The effect of calpain inhibitor-I on copper oxide nanoparticle-induced damage and cerebral ischemia-reperfusion in a rat model(2024) Karimkhani, Hadi; Shojaolsadati, Paria; Yiğitbaşı, Türkan; Kolbaşı, Bircan; Emekli, NeslinThis study aimed to investigate the effects of the calpain inhibitor N-Acetyl-Leu-Leu-norleucinal (ALLN) on neuroapoptotic cell damage caused by Copper Oxide Nanoparticles (CuO-NP) and exacerbation of damage through brain ischemia/reperfusion (I/R) in a rat model. Male Wistar Albino rats (n=80) were divided into eight groups: Control, I/R, CuO-NP, CuO-NP+I/R, I/R+ALLN, CuO-NP+ALLN, CuO-NP+I/R+ALLN, and DMSO. Biochemical markers (MBP, S100B, NEFL, NSE, BCL-2, Cyt-C, Calpain, TNF-?, Caspase-3, MDA, and CAT) were measured in serum and brain tissue samples. Histological examinations (H&E staining), DNA fragmentation analysis (TUNEL) were performed, along with Caspase-3 assessment. The ALLN-treated groups exhibited significant improvements in biochemical markers and a remarkable reduction in apoptosis compared to the damaged groups (CuO-NP and I/R). H&E and Caspase-3 staining revealed damage-related morphological changes and reduced apoptosis in the ALLN-treated group. However, no differences were observed among the groups with TUNEL staining. The findings suggest that ALLN, as a calpain inhibitor, has potential implications for anti-apoptotic treatment, specifically in mitigating neuroapoptotic cell damage caused by CuO-NP and I/R.Öğe The effects of pregabalin on gastric ulcer formation and antioxidant parameters(Osmangazi University, 2020) Kaygısız, Bilgin; Aydın, Şule; Yıldırım, Cafer; Karimkhani, Hadi; Öner, Setenay; Kılıç, Fatma SultanPregabalin, a drug used in epilepsy, anxiety, neuropathic pain is reported to have analgesic effects in inflammatory pain. We aimed to investigate whether pregabalin have gastric side effects and to compare with a non steroidal antiinflammatory drug (NSAID) in rats. The effects of pregabalin on antioxidant levels, which are suggested to protect against gastric mucosal damage were also studied. Pregabalin 30, 50, 100 mg/kg, indomethacin 5 mg/kg (reference-NSAID), saline (control group) were administered orally for 10 days. At the end of 10 day treatment, rats were sacrificed, gastric tissues were removed out, mucus secretion was determined spectrophotometrically, ulcer index was scored from score 0:(no-petechia) to score 3:(petechia>5mm). Also, to evaluate the antioxidant effects of pregabalin, malondialdehyde (MDA) levels, catalase and superoxide dismutase (SOD) activities in gastric tissue were studied. Pregabalin 50 mg/kg and 100 mg/kg similar to indomethacin significantly reduced mucus secretion and increased ulcer index compared to control while pregabalin 30 mg/kg did not. Pregabalin 30 mg/kg and 100 mg/kg decreased SOD and catalase levels. Pregabalin 100 mg/kg dose increased MDA levels. 50 mg/kg and 100 mg/kg pregabalin showed gastric side effects as reduced mucus secretion and ulcer formation similar to indomethacin and 30 mg/kg pregabalin may be reasonable dose without showing gastric side effects. Pregabalin 50 mg/kg seems to have enhancing effects on antioxidant levels.
