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ŞENER, AZİZE

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ŞENER

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AZİZE

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Now showing 1 - 3 of 3
  • PublicationOpen Access
    The Effect of Algan Hemostatic Agent (AHA) on Wound Healing
    (MARMARA UNIV, INST HEALTH SCIENCES, 2020-09-04) ŞEN, ALİ; Aksoy, Halil; Sener, Azize; Akakin, Dilek; Sen, Ali; Ozakpinar, Ozlem Bingol; Ozcan, Sinemcan; Simsek, Ahmet Kaan; Sekerler, Turgut; Guzel, Sevket Ergun; Midi, Ahmet
    Objective: The Algan Hemostatic Agent (AHA) is a novel herbal originated blood stopper. The aim of this study is to investigate the effect of AHA on wound healing on excisional wound model in rats. Methods: In this study, 54 adult Wistar albino rats were used. Rats were divided into 3 groups (saline, Madecassol (R) and AHA). Each group was then divided into 3 subgroups as the 3rd, 7th and 14th days. Two wounds were created in the dorsal thoracic region of the rats. One of the lesions was used for histopathological examinations and the other for hydroxyproline measurement. In order to evaluate the wound healing, wound area were measured during the whole treatment period and animals were sacrificed at the end of the 3rd, 7th and 14th days and tissue samples were taken for the determination of hydroxyproline levels. Results: AHA treatment did not cause significant difference in hydroxyproline level on days 3, 7, 14. The contraction percentage of wound area was higher in the AHA group on day 7 than that of the control group. However, the difference was not statistically significant (p>0.05). On days 3 and 14, no significant difference was detected in the contraction percentage of wound area between the control and the AHA groups. AHA and Madecassol (R) results of epidermis regeneration on the 14th day, neutrophil infiltration on the 7th day and edema on the 3rd, 7th and 14th days were different in terms of histopathological parameters compared to the control group. Conclusion: Despite good histological findings, AHA did not significantly accelerate wound healing, but did not adversely affect wound healing as well.
  • Publication
    Montelukast inhibits caspase-3 activity and ameliorates oxidative damage in the spinal cord and urinary bladder of rats with spinal cord injury
    (ELSEVIER SCIENCE INC, 2012) ŞENER, AZİZE; Ersahin, Mehmet; Cevik, Ozge; Akakin, Dilek; Sener, Azize; Ozbay, Latif; Yegen, Berrak C.; Sener, Goksel
    Spinal cord injury (SCI) leads to an inflammatory response that generates substantial secondary damage within the tissue besides the primary damage. Leukotrienes are biologically active 5-lipoxygenase products of arachidonic acid metabolism that are involved in the mediation of various inflammatory disorders including SCI. In this study, we investigated the possible protective effects of montelukast, a leukotriene receptor blocker, on SCI-induced oxidative damage. Wistar albino rats (n = 24) were divided randomly as control, vehicle- or montelukast (10 mg/kg, ip)-treated SCI groups. To induce SCI, a standard weight-drop method that induced a moderately severe injury at T10 was used. Vehicle or montelukast were administered to the injured animals 15 min after injury. At seven days post-injury, neurological examination was performed and rats were decapitated. Blood samples were taken to evaluate leukotriene 134 levels, and pro-inflmamatory cytokines (TNF-alpha, IL-1 beta) while in spinal cord and urinary bladder samples malondialdehyde (MDA), glutathione (GSH), luminol chemiluminescence (CL) levels and myeloperoxidase (MPO) and caspase-3 activities were determined. Tissues were also evaluated histologically. SCI caused significant decreases in tissue GSH, which were accompanied with significant increases in luminol CL and MDA levels and MPO and caspase-3 activities, while pro-inflammatory cytokines in the plasma were elevated. On the other hand. montelukast treatment reversed these parameters and improved histological findings. In conclusion, SCI caused oxidative tissue injury through the activation of pro-inflammatory mediators and by neutrophil infiltration into tissues, and the neuroprotective and antiapoptotic effects of montelukast are mediated by the inhibition of lipid peroxidation, neutrophil accumulation and proinflammatory cytokine release. Moreover, montelukast does not only exert antioxidant and antiapoptotic effects on the spinal cord, but it has a significant impact on the bladder tissue damage secondary to SCI. (C) 2012 Elsevier Inc. All rights reserved.
  • Publication
    Obestatin alleviates subarachnoid haemorrhage-induced oxidative injury in rats via its anti-apoptotic and antioxidant effects
    (TAYLOR & FRANCIS LTD, 2013) ŞENER, AZİZE; Ersahin, Mehmet; Ozsavci, Derya; Sener, Azize; Ozakpinar, Ozlem Bingol; Toklu, Hale Zerrin; Akakin, Dilek; Sener, Goksel; Yegen, Berrak C.
    Objective: The aim was to investigate the putative anti-inflammatory and anti-apoptotic effect of obestatin in a rat model of subarachnoidal haemorrhage (SAH). Methods: To induce SAH, rats were injected with 0.3 mL blood into their cisterna magna. At 48 hours rats were decapitated after neurological examination. Blood-brain barrier (BBB) permeability, brain water content, oxidative stress markers and histological analysis were done in brain tissue. Results: The results showed that neurological examination scores were increased in the SAH group and, moreover, BBB permeability was impaired and oedema formed. SAH resulted in increased levels of plasma tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-6 levels and caspase-3 activity. Lipid peroxidation and protein oxidation levels and myeloperoxidase activity were all increased in the brain tissue, with concomitant decreases in antioxidant enzymes. On the other hand, SAH-induced neurological impairment and oxidative brain injury were ameliorated in the obestatin-treated group. Conclusion: The present study provides the first evidence that peripheral administration of obestatin exerts potent anti-inflammatory and neuroprotective effects in SAH-induced oxidative damage by maintaining a balance in oxidant-antioxidant status through the augmentation of endogenous antioxidants and the inhibition of pro-inflammatory mediators.