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1

Evaluation of PECAM-1 and p38 MAPK expressions in cerebellum tissue of rats treated with caffeic acid phenethyl ester: a biochemical and immunohistochemical study

100%
Çetin A., Deveci E.
Folia Morphologica
|
2019
|
tom 78
|
nr 2
Background: This study aimed to investigate the antioxidative and anti-inflammatory effects of caffeic acid phenethyl ester (CAPE) on damage caused to cerebellum tissue by diffuse traumatic head trauma via biochemical, histopathologic, and immuno-histochemical methods. Materials and methods: Male Sprague-Dawley (300–350 g) rats were subjected to traumatic brain injury with a weight-drop device (300 g/1 m weight-height impact). Twenty-four adult rats were randomly divided into three equal groups of 8, including a control group, traumatic brain injury (TBI) group, and TBI + CAPE treatment group (10 μmoL/kg/i.p.). Cerebellum tissue samples taken from anterior lobe from all rats were taken 7 days after traumatic injury and were subjected to biochemical and histopathological analysis, as well as immunohistochemical analysis for platelet endothelial cell adhesion molecule-1 (PECAM-1) and phosphate 38-mitogen-activated protein kinase (p38 MAPK). Results: In the TBI group, the granular layer had dilatation and haemorrhage in the capillary vessels and inflammatory cell infiltration around the periphery of the blood vessels. In the TBI + CAPE group, the small capillaries in the white matter were slightly dilated, there were no inflammatory cells, and dense chromatin/ granular cells were observed in the granular layer. Also in the TBI + CAPE group, the Purkinje cells of the ganglion cell layer had ovoid nuclei, were chromatin-rich, and their extensions protruded to the molecular layer. CAPE is thought to regulate inflammation, cell damage, and angiogenetic development by affecting the PECAM-1 and p38 MAPK proteins. Conclusions: These proteins are key modulators of endothelial integrity and neuroinflammation in vessels in response to endothelial damage as well as of the proinflammatory response in the cerebellum in response to traumatic damage. (Folia Morphol 2019; 78, 2: 221–229)
2

Expression of vascular endothelial growth factor and glial fibrillary acidic protein in a rat model of traumatic brain injury treated with honokiol: a biochemical and immunohistochemical study

100%
Cetin A., Deveci E.
Folia Morphologica
|
2019
|
tom 78
|
nr 4
Background: Traumatic brain injury (TBI) leads to neuronal damage and neurological dysfunction. The aim of our study was to investigate the antioxidative effect of honokiol on TBI in rats with biochemical, histopathological and immunohistochemical methods. Materials and methods: Sprague–Dawley rats were subjected to TBI with a weight-drop device using 300 g/1 m weight/height impact. Forty-five rats were divided into three groups as control group, TBI group and TBI + honokiol group (5 mg/kg/day, i.p.). Honokiol (5 mg/kg) dissolved in dimethyl sulfoxide (DMSO) was intraperitoneally administered to rats for 7 days after the trauma. At the end of experiment, blood samples were taken from the animals and analysed with various biochemical markers. Results: Histopathological examination of the trauma group revealed some degenerated pyramidal cells, dilatation and congestion in blood vessels, hyperplasia in endothelial cells, inflammatory cell infiltration around the vein and disruptions in glial extensions. In TBI + honokiol group, pyramidal neurons showed a decrease in degeneration, slight dilatation in blood vessels, improvement of endothelial cells towards the lumen, and reduction of inflammatory cells in the vessel. In TBI + honokiol group, vascular endothelial growth factor expression was positive in the endothelial and few inflammatory cells of the mildly dilated blood vessels. In the blood brain barrier deteriorated after trauma, it was observed that the glial foot processes were positive expression and extended to the endothelial cells in the TBI + honokiol group. Conclusions: Glial fibrillary acidic protein expression showed a positive reaction in these processes. Considering the important role of antioxidants and inflammatory responses in cerebral damage induced by traumatic head injury, honokiol is thought to be important in decreasing lipid peroxidation, protecting the membrane structure of blood brain barrier, degeneration of neurons and glial cells. (Folia Morphol 2019; 78, 4: 684–694)
3

Histopathological changes in the choroid plexus after traumatic brain injury in the rats: a histologic and immunohistochemical study

81%
Ozevren H., Deveci E., Tuncer M. C.
Folia Morphologica
|
2018
|
tom 77
|
nr 4
Background: Traumatic brain injury (TBI) is in part associated with the disruption of the blood-brain barrier. In this study, we analysed the histopathological changes in E-cadherin and vascular endothelial growth factor (VEGF) expression after TBI in rats. Materials and methods: The rats were divided into two groups as the control and the trauma groups. Sprague-Dawley rats were subjected to TBI with a weight-drop device using 300 g/1 m weight-height impact. After 5 days of TBI, blood samples were taken under ketamine hydroxide anaesthesia and biochemical analyses were performed. The control and trauma groups were compared in terms of biochemical values. Results: There was no change in glutathione (GSH) levels and blood-brain barrier permeability. However, malondialdehyde (MDA) and myeloperoxidase (MPO) activity levels increased in the trauma group. In the histopathological examination, choroid plexus in the lateral ventricle, near the pia mater membrane, was removed. In the traumatic group, some of epithelial cells were hyperplasic. Some of them were peeled off the apical surface and had local degeneration. Conclusions: In addition, we observed congestion in capillary vessels and mononuclear cell infiltration around the vessels. After TBI, the increase in VEGF levels, vascular permeability, and interaction with VEGF receptors in endothelial cells lead to oedema of the vessel wall. On the other hand, E-cadherin expression decreased in the tight-junction structures between epithelial cells and basal membrane, resulting in an increase in cerebrospinal fluid in the intervillous area. (Folia Morphol 2018; 77, 4: 642–648)
4

Effects of alloplastic graft material combined with a topical ozone application on calvarial bone defects in rats

71%
Lacin N., Izol B. S., Gokalp Ozkormaz E., Deveci B., Deveci E.
Folia Morphologica
|
2020
|
tom 79
|
nr 3
Background: This study presents the evaluation of the damage in the bone tissue resulting from a calvarial defect in rats and the efficiency of exposure to an ozone application with an alloplastic bone graft on the calvarial bone damage. Materials and methods: Wistar male rats (n = 56) were divided into four groups: a control group (n = 14), defect and ozone group (n = 14), defect and graft group (n = 14), and defect, graft, and ozone group (n = 14). Under anaesthesia, a circular full-thickness bone defect was created in all groups, and the experimental groups were further divided into two sub-groups, with 7 rats in each group sacrificed at the end of the 4th and 8th weeks. Bone samples were dissected, fixed in 10% formalin solution, and decalcified with 5% ethylene-diamine-tetraacetic acid (EDTA). After the routine follow-up on tissues, immunostaining of osteopontin and osteonectin antibodies was applied to sections and observed under a light microscope. Results: The control group exhibited osteopontin and osteonectin expression in fibroblasts and inflammatory cells at the end of the 4th week with an acceleration at the 8th week. Ozone administration elucidated new trabecular bone formation by increasing osteoblastic activity. Lastly, our observations underscore that a combination of allograft and ozone application increased the osteoblast, osteocyte, and bone matrix development at the 4th and 8th weeks. Conclusions: Exposure to an ozone application with an alloplastic bone graft on calvarial bone damage may induce osteoblastic activity, matrix development, mature bone cell formation, and new bone formation in rats. (Folia Morphol 2020; 79, 3: 528–547)
5

Effects of nicotine administration in rats on MMP2 and VEGF levels in periodontal membrane

61%
Deveci B., Ayna B., Tacir I. H., Deveci E., Tuncer M. C., Pala A.
Folia Morphologica
|
2018
|
tom 77
|
nr 3
Background: Nicotine is associated with increased incidence of periodontal disease and poor response to therapy. This article aimed at identifying the expression of matrix metalloproteinases 2 (MMPs2) and vascular endothelial growth factor (VEGF) proteins on extracellular matrix, fibrous distribution and angiogenetic development in periodontitis caused by nicotine effects on periodontal membrane. Materials and methods: In this experimental study, rats were divided into nicotine and control groups. While the rats in the nicotine group (n = 6) were administered 2 mg/kg nicotine sulphate for 28 days, the animals in the control group (n = 6) were only administered 1.5 mL physiologic saline solution subcutaneously for 28 days. Results: Histological sections were prepared and immunohistochemically stained for MMP2 and VEGF. The sections stained with Trichrome-Masson were observed under light microscope. VEGF and MMP2 immunoreactivity of periodontal gingiva and dentin was assessed by immunohistochemical staining. Conclusions: Nicotine reduces MMP production, disrupts collagen synthesis and causes periodontitis. We observed that nicotine increases periodontitis by disrupting periodontal membrane and prevents tooth to anchor in dental alveoli by disrupting epithelial structure. (Folia Morphol 2018; 77, 3: 471–477)
6

Investigation of antioxidant effects of rosmarinic acid on liver, lung and kidney in rats: a biochemical and histopathological study

51%
Oguz A., Boyuk A., Ekinci A., Alabalik U., Turkoglu A., Tuncer M. C., Ekingen A., Deveci E., Gulturk B., Aday U.
Folia Morphologica
|
2020
|
tom 79
|
nr 2
Background: The aim of the study was to investigate the protective effects of rosmarinic acid in rats exposed to hepatic ischaemia/reperfusion (I/R) injury. Materials and methods: Thirty-two rats were randomly classified into four groups of 8 rats each: laparotomy without medication, rosmarinic acid (dose of 50 mg/kg via oral gavage) followed by laparotomy, laparotomy followed by hepatic I/R, and hepatic I/R with rosmarinic acid. Serum aspartate aminotransferase, alanine aminotransferase, and malondialdehyde levels and total oxidant activity and total antioxidant capacity levels of the liver, lung, and kidney were assessed. The histopathologic assessment was also performed. Results: Rosmarinic acid significantly reduced liver function test parameters and decreased oxidative stress and abnormal histopathologic findings in the liver. The oxidative stress in the lung significantly increased in the I/R group but significantly decreased in the I/R + rosmarinic acid group due to the addition of rosmarinic acid. Rosmarinic acid led to no reduction in oxidative stress in kidney following hepatic I/R injury. There were no statistically significant differences among the groups regarding histopathologic changes in kidney and lung sections. Conclusions: Rosmarinic acid has antioxidant properties and is an effective hepatoprotective agent. However, although rosmarinic acid provides useful effects in the lung by increasing antioxidant capacity and reducing oxidative stress after I/R injury, it does not ameliorate histopathologic changes. These findings suggest that rosmarinic acid is likely to provide favourable outcomes in the treatment of hepatic I/R injury. (Folia Morphol 2020; 79, 2: 288–295)
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