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Öğe Cathepsin K and survivin in a collar-induced early atherosclerosis model(Blackwell Publishing, 2006) Islekel, H.; Reel, B.; Oktay, G.; Ozkaya, A.; Sozer, G. Ozsarlak; Kerry, Z.Öğe Diverse effects of taurine on vascular response and inflammation in GSH depletion model in rabbits(Verduci Publisher, 2016) Ozsarlak-Sozer, G.; Sevin, G.; Ozgur, H. H.; Yetik-Anacak, G.; Kerry, Z.OBJECTIVE: A reduction in GSH and an increase in free radicals are observed in inflammatory diseases, indicating oxidative stress. Taurine protects cells from the cytotoxic effects of inflammation. There have been limited studies to date evaluating the effect of taurine in oxidative stress-induced vascular dysfunction and its role in vascular inflammatory diseases. Therefore, we aimed to investigate the effect of taurine on the regulation of vascular tonus and vascular inflammatory markers in rabbit aortae and carotid arteries in oxidative stress-induced by GSH depletion. MATERIALS AND METHODS: Rabbits were treated subcutaneously with buthionine sulfoximine (BSO), GSH-depleting compound and/or taurine. Cumulative concentration-response curves for acetylcholine (ACh), phenylephrine and 5-hydroxytriptamine (5-HT) were constructed with or without N-omega-nitro-L-arginine (LNA) in the carotid artery and aorta rings. Immunohistochemical staining was performed for TNF-alpha and IL-1 beta. RESULTS: BSO increased ACh-induced NOdependent relaxations, phenylephrine-induced contractions in the carotid artery and 5-HT induced-contractions in both the carotid artery and the aorta. BSO decreased EDHF dependent relaxations only in the aorta. ACh-induced NO-dependent relaxations and augmented contractions were normalized by taurine. BSO increased TNF-alpha expressions in both carotid arteries and aortas, which were reversed by taurine. The BSO-induced increase in IL-1 beta was reversed by taurine only in aortae. CONCLUSIONS: Treatment with BSO resulted in vascular reactivity changes and increased immunostaining of TNF-alpha in mainly carotid arteries in this model of oxidative stress. The effect of taurine on BSO-induced vascular reactivity changes varied depending on the vessel. The inhibition of the increase in TNF-alpha expression by taurine in both carotid arteries and aortae supports the proposal that taurine has a beneficial effect in the treatment of inflammatory diseases such as atherosclerosis.Öğe The effects of calcium channel blockers are not related to their chemical structure in the collar model of the rabbit(Cambridge Med Publ, 2007) Yasa, M.; Kerry, Z.; Reel, B.; Anacak, G. Yetik; Ertuna, E.; Ozer, A.Placing a silicone collar around the rabbit carotid artery induces intimal thickening, an early stage in atherosclerosis and restenosis. We investigated whether treatment with oral pranidipine, a new potent, long lasting dihydropyridine calcium channel blocker (CCB), inhibited collar-induced intimal thickening in addition to the changes in vascular reactivity usually observed in this model. Pranidipine treatment did not inhibit collar-induced intimal thickening. Placing the collar around the carotid artery resulted in the characteristic changes in vascular reactivity, such as increased sensitivity to 5-hydroxytryptamine. Treatment with N-omega-nitro-L-arginine (100 mu M) and pranidipine, however, did not affect collarinduced changes in vascular reactivity. From results of this and previous studies, we conclude that pranidipine does not prevent collar-induced intimal thickening or collar-induced changes in vascular reactivity. Not all CCBs prevent collarinduced intimal thickening, suggesting that the effects of these agents are not related to their chemical structure and/or their calcium channel-blocking actions.Öğe The effects of chronic ETA/ETB receptor blockade in the isolated rabbit aorta(Blackwell Publishing, 2006) Reel, B.; Oktay, G.; Sozer, G. Ozsarlak; Kerry, Z.Öğe Effects of fluvastatin on H2O2-induced oxidative stress in carotid arteries of rabbit(Blackwell Publishing, 2006) Sevin, G.; Gokce, G.; Sozer, G. Ozsarlak; Yasa, M.; Kerry, Z.Öğe Taurine supplementation protects lens against glutathione depletion(Verduci Publisher, 2021) Sevin, G.; Kerry, Z.; Sozer, N.; Ozsarlak-Sozer, G.OBJECTIVE: Cataract which is defined as opacification of eye lens forms approximately 40% of total blindness causes all through the world. Age is the biggest risk factor for cataracts and oxidative stress is known to be one of the most important factors causing cataract formation. Age-related nuclear cataract (ARN) is associated with a loss of glutathione in the center of the lens. Taurine is an important antioxidant in lens tissue. Although, there is a high amount of taurine in lenses in early life, its concentration declines with age. In this study, we aimed to investigate the effects of supplemental taurine in lens tissues in an in vivo oxidative stress model which is induced by glutathione depletion to mimic ARN. MATERIALS AND METHODS: Glutathione depletion was induced in rabbits subcutaneously with l-Buthionine -(S,R)-sulfoximine (BSO)- a glutathione inhibitor and the rabbits were treated with taurine. Total GSH, reduced GSH, GSH/GSSG ratio and MDA levels were measured. RESULTS: BSO lowered the reduced GSH and total GSH levels and GSH/GSSG ratio. Taurine reversed these effects. On the other hand, BSO enhanced MDA level which is normalized by taurine. CONCLUSIONS: These findings suggest that glutathione depletion with BSO may be a useful model to mimic ARN and dietary intake of taurine, may have an important role in decelerating the process of cataract formation.Öğe Taurine suppresses oxidative stress-potentiated expression of lectin-like oxidized low-density lipoprotein receptor and restenosis in balloon-injured rabbit iliac artery(Wiley-Blackwell, 2011) Gokce, G.; Ozsarlak-Sozer, G.; Oran, I.; Oktay, G.; Ozkal, S.; Kerry, Z.1. In endothelial cells, the major receptor for the binding and internalization of oxidized low-density lipoprotein (LDL) is the lectin-like oxidized LDL receptor (LOX-1). The aim of the present study was to investigate the effects of taurine on intimal thickening and LOX-1 expression under normal and oxidative conditions.Öğe Telomeric restriction analysis of vascular smooth muscle cells following balloon angioplasty in rabbits(Springer, 2009) Ozsarlak-Sozer, G.; Kerry, Z.; Oran, I.; Gokce, G.; Tosun, M.; Bechard, L.; Reel, B.; Yasa, M.; Lebe, B.; Topcu, Z.G. OZSARLAK-SOZER, Z. KERRY, I. OR-AN, G. GOKCE, M. TOSUN, L. BECHARD, B. REEL, M. YASA, B. LEBE and Z. TOPCU. Telomeric restriction analysis of vascular smooth muscle cells following balloon angioplasty in rabbits. J Physiol Biochem, 65 (3), 243-250, 2009. Intimal hyperplasia due to smooth muscle cell proliferation and migration has been reported to be responsible for the pathogenesis of atherosclerosis and restenosis, manifested following balloon angioplasty. In this study, we employed the balloon angioplasty model to study telomere length regulation in proliferating vascular smooth muscle cells. Our results showed that balloon angioplasty in iliac arteries resulted in intimal hyperplasia due to proliferation of the smooth muscle cells and small size telomeric restrictional fragments were evident in injured arteries.Öğe Telomeric restriction analysis of vascular smooth muscle cells following balloon angioplasty in rabbits(Springer, 2009) Ozsarlak-Sozer, G.; Kerry, Z.; Oran, I.; Gokce, G.; Tosun, M.; Bechard, L.; Reel, B.; Yasa, M.; Lebe, B.; Topcu, Z.G. OZSARLAK-SOZER, Z. KERRY, I. OR-AN, G. GOKCE, M. TOSUN, L. BECHARD, B. REEL, M. YASA, B. LEBE and Z. TOPCU. Telomeric restriction analysis of vascular smooth muscle cells following balloon angioplasty in rabbits. J Physiol Biochem, 65 (3), 243-250, 2009. Intimal hyperplasia due to smooth muscle cell proliferation and migration has been reported to be responsible for the pathogenesis of atherosclerosis and restenosis, manifested following balloon angioplasty. In this study, we employed the balloon angioplasty model to study telomere length regulation in proliferating vascular smooth muscle cells. Our results showed that balloon angioplasty in iliac arteries resulted in intimal hyperplasia due to proliferation of the smooth muscle cells and small size telomeric restrictional fragments were evident in injured arteries.
