Melatonin and oxidation

[No abstract available

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

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

Adenozin ve adenozin A1 reseptör agonisti CPA'nın lokal uygulanımı sıçan ince barsak hasarına karsı koruyucu etkiler göstermektedir

Amaç: Adenozin ve A1 adenozin reseptör (A1AR) agonistleri, çeşitli dokuların reperfüzyon hasarına karşı koruyucu etkilere sahiptir. Çalışmanın amacı, sıçan ince barsağının reperfüzyon harabiyetinde adenozin ve A1AR agonistinin lokal uygulanmasının etkilerini incelemekti. Gereç ve Yöntemler: Sıçanlar herbiri altı hayvan içeren beş gruba rastgele olarak aşağıdaki gibi ayrıldı: sham kontrol; iskemi-reperfüzyon (I/R) kontrol; adenozin + I/R; A1AR agonisti 2-kloro-N6-siklopentiladenozin (CPA) + I/R ve A1AR antagonisti 8-siklopentil-1,3-dipropilksantin (DPCPX) + adenozin + I/R. ?laçların abdominal boşluğa 5 dk boyunca lokal uygulanmasını takiben barsak I/R’u, süperiyor mezenter arterin 30 dk klempe edilmesi ve sonrasındaki 180 dk lık reperfüzyon dönemi ile sağlandı. Daha sonra terminal ileum örnekleri toplandı ve karbakole olan kasılma yanıtlarını ölçmek için hızlıca izole organ banyosuna alındı. Ayrıca malondialdehid (MDA) ve indirgenmiş glutatyon (GSH) düzeylerini ölçmek için de ek doku örnekleri alındı. Bulgular: I/R, lipid peroksidasyonunu ileri düzeyde yükseltirken, indirgenmiş glutatyonu düşürdü. Sham kontrol grubuyla karşılaştırıldığında, kasılma yanıtları I/R grubunda ciddi düzeyde azaldı. Adenozin veya CPA ön tedavisi, sadece lipit peroksidasyonunu azaltmakla kalmadı aynı zamanda kasılma yanıtı ve GSH düzeyini de ileri derecede iyileştirdi. Bu yararlı etkilerin, A1AR anatgonisti DPCPX ön tedavisi ile ortadan kalktığı gözlendi. Sonuç: Elde ettiğimiz kanıtlar, sistemik uygulanımının yanı sıra, adenozin ve A1AR agonisti CPA’nın lokal uygulanmasının da iskemik barsak harabiyetini, en azından oksidatif stresi azaltarak ve antioksidan savunmayı güçlendirerek iyileştirdiğini önermektedir.Objective: Adenosine and adenosine A1 receptor (A1AR) agonists have potential protective effects against reperfusion injury in variety of tissues. The purpose of the present study was to investigate possible effects of topical administration of adenosine and A1AR agonist on reperfusion-induced small intestinal injury in rat. Materials and Methods: Rats were randomized to five groups each including six as following: sham-operated control; ischemia-reperfusion (I/R) control; adenosine + I/R; A1AR agonist 2-chloro-N6-cyclopentyladenosine (CPA) + I/R; and A1AR antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) + adenosine + I/R. Following topical administration of the drugs into abdominal cavity for 5 min, intestinal I/R was established by clamping superior mesenteric artery (SMA) for 30 minutes followed by 180 min of reperfusion period. Afterwards terminal ileum samples were collected and immediately transferred to isolated organ bath for measuring contractile response to carbachol. Furthermore, additional tissue samples were harvested for measuring the levels of malondialdehyde (MDA) and reduced glutathione (GSH). Results: I/R significantly increased lipid peroxidation while decreasing the GSH. Contractile responses were seriously reduced in I/R group compared to that of the sham control group. Pretreatment with adenosine or CPA not only decreased lipid peroxidation but also ameliorated contractile response and GSH levels remarkably. These beneficial effects were abolished by pretreatment with A1AR antagonist DPCPX. Conclusion: Evidences we collected suggest that besides systemic administration, local application of adenosine and A1AR agonist CPA also attenuate ischemic intestinal injury via, at least, decreasing oxidative stress and enhancing antioxidant defense

The effects of 17 beta estradiol, 17 alpha estradiol and progesterone on oxidative stress biomarkers in ovariectomized female rat brain subjected to global cerebral ischemia

Neuroprotective effects of estrogens and progesterone have been widely studied in various experimental models. The present study was designed to compare possible neuroprotective effects of 17alpha-estradiol, 17beta-estradiol, and progesterone on oxidative stress in rats subjected to global cerebral ischemia. Global cerebral ischemia was induced in ovariectomized female rats by four vessel occlusion for 10 min. Following 72 h of reperfusion, levels of malondialdehyde (MDA, oxidative stress marker), and reduced glutathione (GSH, major endogenous antioxidant) were assessed in hippocampus, striatum and cortex of rats treated with either 17alpha-estradiol, 17beta-estradiol, progesterone or estradiol + progesterone beforehand. Steroid administration ameliorated ischemia-induced decrease in GSH and increase in MDA levels. Our data offers additional evidence that estrogens and progesterone or combination of two exert a remarkable neuroprotective effect reducing oxidative stress. © 2009 Institute of Physiology v.v.i., Academy of Sciences of the Czech Republic, Prague, Czech Republic

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

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

The effects of ethyl pyruvate on cognitive function, oxidative stress, and Na-K ATPase levels in vascular dementia model

WOS: 00038357830019

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

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)

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

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

The Effects of Sirtuin 1 and Oxidative Stress on Oligodendrocyte Death in Cuprizone-induced Model of Demyelination

WOS: 00038357830018

Sıçan ince barsağının iskemi-reperfüzyonunda 5’-N-etilkarboksiamidoadenozin ön tedavisi kısmi iyileşme sağlamaktadır

Amaç: Adenozin ve adenozin A1 reseptör agonistleri, çeşitli dokuların reperfüzyon harabiyetine karşı önkoşullanma yoluyla koruyucu etkiler göstermektedir. Çalışmanın amacı, sıçan ince bağırsağının reperfüzyon harabiyeti üzerine adenozin A1/A2 reseptör aktivasyonunun etkilerini incelemekti. Yöntemler: Denekler herbiri rastgele sekiz hayvan içeren dört gruba ayrıldı: sham kontrol, iskemi-reperfüzyon kontrol, 5’-N-etilkarboksiamidoadenozin (NECA) (non-selektif A1 /A2 agonisti, 0.1 mg/kg, i.v.) tedavili iskemi-reperfüzyon ve teofilin (non-selektif A1 /A2 antagonisti, 20 mg/kg, i.v.) tedavili iskemi-reperfüzyon. Tedaviler iskemi yapılmadan 5 dk önce uygulandı. Süperiyor mezenter arter 30 dk klempe edildikten sonra reperfüzyon dönemi 180 dk sürdü. Terminal ileum segmentlerinin, KCl, karbakol ve substans P’ye olan kasılma yanıtlarının kaydedilmesinin yanısıra, dokuların miyeloperoksidaz, malondialdehit ve indirgenmiş glutatyon miktarları da ölçüldü. Bulgular: İskemi, nötrofil infiltrasyonu ve lipid peroksidasyonunu ileri düzeyde yükseltirken aynı zamanda indirgenmiş glutatyonu düşürdü. Sham control grubuy- la karşılaştırıldığında, kasılma yanıtları iskemi-reperfüzyon grubunda ciddi düzeyde azaldı. NECA ön tedavisi, doku indirgenmiş glutatyon miktarını ileri derecede düzeltti ve ayrıca iskemi-reperfüzyon sonucu azalmış kasılma yanıtını kısmen iyileştirdi. Teofilin ile ön tedavi ise herhangi koruyucu bir etki göstermedi. Sonuç: Adenozin A1 /A2 reseptör aktivasyonunun, iskemi sonucu gelişen bağırsak kasılma bozukluğuna karşı kısmi koruma sağladığını ve ayrıca bu korumanın, indirgenmiş glutatyon düzeyinin fizyolojik seviyede tutulması yolu ile muhtemelen gerçekleştiğine dair ek kanıt önermekteyiz.Objectives: Adenosine and adenosine A1 receptor agonists exert protective effects against reperfusion injury in different tissues by mediating preconditioning. The aim of the present study was to examine the effects of adenosine A1 /A2 receptor activation on reperfusion-induced small intestinal injury in rat. Methods: Animals were randomized into four groups each including eight as following: sham control, ischemia-reperfusion control, 5’-N-ethylcarboxamidoadenosine (NECA) (non-selective A1 /A2 agonist, 0.1 mg/kg, i.v.)-treated I/R, and theophylline (non-selective A1 /A2 antagonist, 20 mg/kg, i.v.)-treated I/R groups. The treatments were administered 5 min before inducing ischemia in which superior mesenteric artery was clamped for 30 min followed by 180 min of reperfusion pe- riod. Myeloperoxidase, malondialdehyde, and reduced glutathione contents of terminal ileum samples were measured besides recording contractile responses to KCl, carbachol and substance P. Results: Ischemic insult significantly increased neutrophil infiltration and lipid peroxidation while decreasing the reduced glutathione. Contractile responses were seriously reduced in I/R group compared to that of the sham control group. NECA pretreatment alleviated the tissue content of reduced glutathione remarkably besides providing partial amelioration of I/R-reduced contractile response, while theophylline pretreatment had no any protective effect. Conclusion: We offer additional evidence that activation of A1 /A2 adenosine receptors provides partial protection against ischemia-induced intestinal contractile dysfunction possibly through maintaining reduced glutathione content at physiological levels