Can Erzik

Publications (24) View all

• Conference Proceeding: Antioxidant effects of alpha-lipoic acid and n-acetyl cysteine on acrylamide-induced gonotoxicity in male rats

  Meral Yüksel, A.Özer Şehirli, Enise Çavuşoğlu-Dalgıçdir, Olgu Enis Tok, Can Erzik, Feriha Ercan, Goncagül Haklar
  4th International Congress on Cell Membranes and Oxidative Stress: Focus on Calcium Signaling and TRP Channels, Turkey; 06/2012
• Article: Alpha Lipoic Acid Alleviates Oxidative Stress and Preserves Blood Brain Permeability in Rats with Subarachnoid Hemorrhage

  Mehmet Erşahin, Hale Z. Toklu, Şule Çetinel, Meral Yüksel, Can Erzik, M. Zafer Berkman, Berrak Ç. Yeğen, Göksel Şener
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  ABSTRACT: The neuroprotective effect of alpha lipoic acid (ALA; 100mg/kg, po), a dithiol antioxidant, on experimentally induced subarachnoid hemorrhage (SAH) was assessed in Wistar albino rats. Neurological examination scores recorded at the 48thh of SAH induction were increased in SAH groups, which were accompanied with significant increases in the formation of reactive oxygen species, DNA fragmentation ratios, malondialdehyde levels and myeloperoxidase activity, while significant decreases in the brain glutathione content and Na+, K+-ATPase activity were observed. On the other hand, ALA treatment reversed all these biochemical indices as well as SAH-induced histopathological alterations. Increased brain edema, impaired blood-brain-barrier permeability and neurological scores were also improved by ALA treatment. The results demonstrate that ALA exerts neuroprotective effects via the enhancement of endogenous antioxidant enzyme activity, the inhibition of neutrophil accumulation and free radical generation, suggesting a therapeutic potential in reducing secondary injury after SAH in patients.
  Neurochemical Research 04/2012; 35(3):418-428. · 2.24 Impact Factor
• Article: Meloxicam exerts neuroprotection on spinal cord trauma in rats.

  Tayfun Hakan, Hale Zerrin Toklu, Necat Biber, Hasan Celik, Can Erzik, Ayliz Velioğlu Oğünç, Sule Çetinel, Göksel Sener
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  ABSTRACT: Traumatic injury to the central nervous system results in the delayed dysfunction and neuronal death. Impaired mitochondrial function, generation of reactive oxygen species (ROS), and lipid peroxidation occur soon after traumatic spinal cord injury (SCI), while the activation of compensatory molecules that neutralize ROS occurs at later time points. The aim of the current study was to investigate the putative neuroprotective effect of the COX2 inhibitor meloxicam in a rat model of SCI. In order to induce SCI, a standard weight-drop method that induced a moderately severe injury (100 g/cm force) at T10, was used. Injured animals were given either 2 mg/kg meloxicam or saline 30 min postinjury by intraperitoneal injection. At seven days postinjury, neurological examination was performed and rats were decapitated. Spinal cord samples were taken for histological examination or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and DNA fragmentation. Formation of ROS in spinal cord tissue samples was monitored by using a chemiluminescence (CL) technique. SCI caused a significant decrease in spinal cord GSH content, which was accompanied with significant increases in CL, MDA levels, MPO activity, and DNA damage. On the other hand, meloxicam treatment reversed all these biochemical parameters as well as SCI-induced histopathological alterations. Furthermore, impairment of the neurological functions due to SCI was improved by meloxicam treatment. The present study suggests that meloxicam, reduces SCI-induced oxidative stress and exerts neuroprotection by inhibiting lipid peroxidation, GSH depletion, and DNA fragmentation.
  The International journal of neuroscience 03/2011; 121(3):142-8. · 0.86 Impact Factor
• Article: The anti-inflammatory and neuroprotective effects of ghrelin in subarachnoid hemorrhage-induced oxidative brain damage in rats.

  Mehmet Erşahin, Hale Z Toklu, Can Erzik, Sule Cetinel, Dilek Akakin, Ayliz Velioğlu-Oğünç, Sermin Tetik, Zarife N Ozdemir, Göksel Sener, Berrak C Yeğen
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  ABSTRACT: To elucidate the putative neuroprotective effects of ghrelin in subarachnoid hemorrhage (SAH)-induced brain injury, Wistar albino rats (n = 54) were divided into sham-operated control, saline-treated SAH, and ghrelin-treated (10 microg/kg/d IP) SAH groups. The rats were injected with blood (0.3 mL) into the cisterna magna to induce SAH, and were sacrificed 48 h after the neurological examination scores were recorded. In plasma samples, neuron-specific enolase (NSE), S-100beta protein, TNF-alpha, and IL-1beta levels were evaluated, while forebrain tissue samples were taken for the measurement of malondialdehyde (MDA), glutathione (GSH), reactive oxygen species levels, myeloperoxidase (MPO), Na(+)-K(+)-ATPase activity, and DNA fragmentation ratio. Brain tissue samples containing the basilar arteries were obtained for histological examination, while cerebrum and cerebellum were removed for the measurement of blood-brain barrier (BBB) permeability and brain water content. The neurological scores were impaired at 48 h after SAH induction, and SAH caused significant decreases in brain GSH content and Na(+)-K(+)-ATPase activity, and increases in chemiluminescence, MDA levels, and MPO activity. Compared with the control group, the protein levels of NSE, S-100beta, TNF-alpha, and IL-1beta in plasma were also increased, while ghrelin treatment prevented all SAH-induced alterations observed both biochemically and histopathologically. The results demonstrate that ghrelin alleviates SAH-induced oxidative brain damage, and exerts neuroprotection by maintaining a balance in oxidant-antioxidant status, by inhibiting proinflammatory mediators, and preventing the depletion of endogenous antioxidants evoked by SAH.
  Journal of neurotrauma 03/2010; 27(6):1143-55. · 4.25 Impact Factor
• Article: Neuroprotective effects of alpha-lipoic acid in experimental spinal cord injury in rats.

  Hale Z Toklu, Tayfun Hakan, Hasan Celik, Necat Biber, Can Erzik, Ayliz V Ogunc, Dilek Akakin, Esra Cikler, Sule Cetinel, Mehmet Ersahin, Goksel Sener
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  ABSTRACT: Oxidative stress is a mediator of secondary injury to the spinal cord following trauma. To investigate the putative neuroprotective effect of alpha-lipoic acid (LA), a powerful antioxidant, in a rat model of spinal cord injury (SCI). Wistar albino rats were divided as control, vehicle-treated SCI, and LA-treated SCI groups. To induce SCI, a standard weight-drop method that induced a moderately severe injury (100 g/cm force) at T10 was used. Injured animals were given either 50 mg/kg LA or saline at 30 minutes postinjury by intraperitoneal injection. At 7 days postinjury, neurologic examination was performed, and rats were decapitated. Spinal cord samples were taken for histologic examination or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and DNA fragmentation. Formation of reactive oxygen species in spinal cord tissue samples was monitored by using a chemiluminescence (CL) technique. SCI caused a significant decrease in spinal cord GSH content, which was accompanied with significant increases in luminol CL and MDA levels, MPO activity, and DNA damage. Furthermore, LA treatment reversed all these biochemical parameters as well as SCI-induced histopathologic alterations. Conversely, impairment of the neurologic function caused by SCI remained unchanged. The present study suggests that LA reduces SCI-induced oxidative stress and exerts neuroprotection by inhibiting lipid peroxidation, glutathione depletion, and DNA fragmentation.
  The journal of spinal cord medicine 01/2010; 33(4):401-9. · 2.11 Impact Factor