37 research outputs found

    Kurkumin kronik serebral hipoperfüzyona maruz kalmış overektomili sıçan beyin dokusunda oksidatif stresi azaltmaktadır

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    Giriş: Turmeriğin majör komponenti olan kurkumin hem antioksidan hem de antiinflamatuar aktivite göstermektedir. Çalışmamızda, kronik serebral hipoperfüzyon modelini kullanarak, overleri alınmış dişi sıçan beyininde, kurkuminin oksidatif stresi azaltıp azaltmadığını araştırdık. Gereç ve Yöntem: Kronik serebral hipoperfüzyon, her iki karotid komunis arterin kalıcı ligasyonu ile sağlandı. Denekler (4-6 aylık toplam 30 adet yetişkin Wistar Albino dişi sıçanlar) rastgele üç gruba ayrıldı: sham kontrol, iskemi ve 14 gün boyunca günlük kurkumin (100 mg/kg) verilen iskemi grubu. Ligasyon sonrası 14üncü günde tüm gruplardaki beyin dokularının malondialdehid (MDA) ve indirgenmiş glutatyon (GSH) içerikleri ölçüldü. Bulgular: İskemi, MDA içeriğinin ileri dercede yükselmesine neden olurken GSH seviyesini anlamlı derecede azalttı. Diğer yandan, kurkumin tedavisi iskemik beyin dokusunda anlamlı derecelerde MDA düzeyini düşürerek ve GSH içeriğini yükselterek, değerlerin sham grubundakiler seviyesine geri dönmesini sağladı. Sonuç: Elde ettiğimiz sonuçlar, vasküler demansın deneysel hayvan modeli olan kronik serebral hipoperfüzyonda kurkuminin hem oksidatif stresi hem de lipid peroksidasyonunu azalttığını önermektedir. Altta yatan moleküler mekanizmaların derinlemesine daha fazla araştırılması sonrasında inanıyoruz ki kurkuminin tedavideki verimliliği, klinik uygulamalar için özellikle de vasküler demanslı menopoz sonrası yaşlı kadınlarda test edilmesine layık olacaktır.Introduction: Curcumin, the major constituent of turmeric, exhibits both antioxidant and anti-inflammatory activities. In the present study, we investigated whether or not curcumin reduces oxidative stress in ovariectomized female rat brain by using a model of chronic cerebral hypoperfusion. Materials and Method: Chronic cerebral hypoperfusion was induced by permanent ligation of both common carotid arteries. Animals (a total of 30 adult female Wistar Albino rats, 4-6 months old) were randomly divided into three groups: sham control, ischemia, and ischemia plus daily curcumin treatment (100 mg/kg) for 14 days. At day 14 after the ligation, malondialdehyde (MDA) and reduced glutathione (GSH) contents of brain tissues were measured in all groups. Results: Ischemia caused a significant increase in MDA content but a meaningful decrease in GSH levels. Treatment with curcumin, however, lowered MDA and elevated GSH contents significantly in ischemic brain tissue, bringing their levels back to that of the sham group. Conclusion: Our results suggest that curcumin attenuates both oxidative stress and lipid peroxidation in chronic cerebral hypoperfusion, which is an animal model of vascular dementia. Following further in depth investigations into underlying molecular mechanism(s), we believe that therapeutic efficacy of curcumin deserves to be tested for potential clinical application especially in postmenopausal elderly women suffering from vascular dementia

    The effects of S-nitrosoglutathione on intestinal ischemia reperfusion injury and acute lung injury in rats: Roles of oxidative stress and NF-kB

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    Background: Intestinal ischemia and reperfusion (I/R) induces oxidative stress, inflammatory response, and acute lung injury. S-nitrosoglutathione (GSNO), a nitric oxide donor, has been documented to have protective effects on experimental ischemia models. Aim: The aim of this study was to examine the effect of GSNO on I/R-induced intestine and lung damage and detect the potential mechanisms emphasizing the protective role of GSNO. Methods: Intestinal I/R was induced by occluding the superior mesenteric artery for 30 min followed by reperfusion for 180 min. GSNO was administered intravenously before reperfusion period (0.25 mg/kg). The levels of lipid peroxidation, reduced glutathione, and myeloperoxidase (MPO), histopathological evaluation and immunohistochemical expressions of both nuclear factor KappaB (NF-?B) and inducible nitric oxide (iNOS) in intestine and lung tissues were assessed. Results: Histolopathologic evaluation demonstrated that intestinal I/R induced severe damages in the intestine and the lung tissues. Histopathological scores decreased with GSNO treatment. GSNO treatment reduced lipid peroxidation and MPO levels and inhibited expression of NF-?B and iNOS in the intestine. Conclusion: Our results suggest that GSNO treatment may ameliorate the intestinal and lung injury in rats, at least in part, by inhibiting inflammatory response and oxidative stress. © 2018 Elsevier Lt

    Melatonin provides neuroprotection by reducing oxidative stress and HSP70 expression during chronic cerebral hypoperfusion in ovariectomized rats

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    Oxidative stress is believed to contribute to functional and histopathologic disturbances associated with chronic cerebral hypoperfusion (CCH) in rats. Melatonin has protective effects against cerebral ischemia/reperfusion injury. This effect has mainly been attributed to its antioxidant properties. In the present study, we evaluate the effects of melatonin on chronic cerebral hypoperfused rats and examined its possible influence on oxidative stress, superoxide dismutase (SOD) activity, reduced glutathione (GSH) levels, and heat shock protein (HSP) 70 induction. CCH was induced by permanent bilateral common carotid artery occlusion in ovariectomized female rats. Extensive neuronal loss in the hippocampus at day 14 following CCH was observed. The ischemic changes were preceded by increases in malondialdehyde (MDA) concentration and HSP70 induction as well as reductions in GSH and SOD. Melatonin treatment restored the levels of MDA, SOD, GSH, and HSP70 induction as compared to the ischemic group. Histopathologic analysis confirmed the protective effect of melatonin against CCH-induced morphologic alterations. Taken together, our results document that melatonin provides neuroprotective effects in CCH by attenuating oxidative stress and stress protein expression in neurons. This suggests melatonin may be helpful for the treatment of vascular dementia and cerebrovascular insufficiency. © 2009 John Wiley and Sons A/S

    Chronic treatment with resveratrol, a natural polyphenol found in grapes, alleviates oxidative stress and apoptotic cell death in ovariectomized female rats subjected to chronic cerebral hypoperfusion

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    Objectives: Resveratrol appears to have neuroprotective potential in various animal models of brain disorders including cerebral ischemia and neurodegenerative diseases. Chronic cerebral hypoperfusion is a well-known pathological condition contributing to the neurodegenerative diseases such as vascular dementia. Purpose of the present study is to evaluate the possible therapeutic potential of resveratrol in a model of vascular dementia of ovariectomized female rats. Assessment of the potential was based on the determination of brain oxidative status, caspase-3 level, glial fibrillary acidic protein (GFAP), and neuronal damage on hippocampus and cerebral cortex. Methods: For creating the model of chronic cerebral hypoperfusion, ovariectomized female Wistar rats were subjected to the modified two vessel occlusion method, with the right common carotid artery being occluded first and the left one a week later. Results: At the 15th day following the ligation, neuronal damage was accompanied by the increased immunoreactivities of both GFAP and caspase-3, and significant neurodegeneration was evident in the hippocampus and cortex, all of which were significantly alleviated with resveratrol treatment (10 mg/kg). Biochemical analysis revealed that the resveratrol treatment decreased lipid peroxidation and restored reduced glutathione level as well. Discussion: The collected data of the present study suggest that the administration of resveratrol may provide a remarkable therapeutic benefit for vascular dementia, which is most likely related to the prevention of both apoptotic cell death and oxidative stress. We believe that therapeutic efficacy of resveratrol deserves to be tested for potential clinical application in postmenopausal elderly women suffering from vascular dementia. © 2015 W. S. Maney & Son Ltd 2015

    Ethyl pyruvate prevents from chronic cerebral hypoperfusion via preserving cognitive function and decreasing oxidative stress, caspase 3 activation and IL-1ß level

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    BACKGROUND: One of the important risk factors for dementia is chronic cerebral hypoperfusion (CCH) especially in patients with cerebrovascular disease. OBJECTIVES: In the present study, using rat model of bilateral common carotid artery occlusion, the possible protective effects of ethyl pyruvate (EP) have been explored in terms of memory impairment, oxidative stress, and levels of caspase-3, Na-K ATPase, and IL- 1ß. METHODS: Rats were treated with EP (50 mg/kg, i.p) for 4 weeks. Cognitive function was evaluated by Morris Water Maze (MWM). Both levels of caspase-3 and Na-K ATPase in tissue, IL-1ß in plasma were measured by ELISA method. Status of oxidative stress in brain was assessed by the measurements of the tissue malondialdehyde (MDA) and reduced glutathione (GSH) contents. RESULTS: Results showed that CCH caused a striking impairment of spatial working memory, accompanied with increased levels of MDA and IL-1ß as well as caspase 3 level. The treatment with EP, however, significantly improved the memory impairment. Moreover, the treatment also provided beneficial effects on the disturbances of caspase 3, IL-1ß and MDA. CONCLUSION: This study strongly imply that the EP administration can alleviate the memory impairment observed due to CCH. The protection provided by EP may result from inhibition of inflammatory response, apoptotic processes and oxidative stress. © 2018, Comenius University.Bülent Ecevit Üniversitesi: 2014-26259946-01This study was fi nancially supported by the Bülent Ecevit University (Grant Number: 2014-26259946-01)

    The effect of melatonin on depressive like behaviour, age and S100b levels in diabetic rats

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    3rd International Congress of the Turkish-Neuroendocrinology-Society -- JUN 29-JUL 01, 2018 -- Malatya, TURKEYWOS: 000445952400080Turkish Neuroendocrinol So
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