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1

Neuroprotective effects of allopurinol on spinal cord injury in rats: a biochemical and immunohistochemical study

100%
Baloglu M., Ozkorkmaz E. G.
Folia Morphologica
|
2019
|
tom 78
|
nr 4
Background: Lesion in spinal cord causes a cascade of events such as the apoptosis of neurons and eventually, neurological dysfunction. Neurologic damage developing after acute spinal cord injury is also related with necrosis and free radical formation. Allopurinol, a xanthine oxidase inhibitor, was shown to have protective effects in several studies. B-cell lymphoma 2 (Bcl-2) family proteins regulate apoptosis. Apoptosis causes the death of neuronal cells, particularly neurons and oligodendrocytes in the spinal cord after lesion. Glial fibrillary acidic protein (GFAP) takes part in astrocyte and neuronal interconnection and synaptic transmission. Materials and methods: Male Sprague Dawley rats (n = 30) were divided as control, trauma, and trauma + allopurinol (i.p., 50mg/kg of body weight) groups. Animals were applied a surgical procedure causing spinal cord injury and treated for 7 days then sacrificed under anaesthesia. The spinal cords were dissected, measurements of myeloperoxidase, malondialdehyde and glutathione were performed, remaining parts were fixed in 10% formaldehyde solution for histological and immunohistochemical evaluations. Results: Biochemical results exhibited an increase in myeloperoxidase levels in trauma group but a decrease in the allopurinol treatment group similar to malondialdehyde levels. Degenerative changes in multipolar and bipolar neurons together with apoptotic changes in some glial cells were observed in the trauma group whereas, mild degenerative changes were observed after allopurinol treatment. In the trauma group, negative GFAP expression in multipolar versus bipolar neuronal processes with a reduction in glial processes around blood vessels and positive GFAP expression were observed but, a regular and parallel positive GFAP expression of glial processes around blood vessels in the allopurinol treated group was apparent. Trauma group depicted a positive Bcl-2 expression in glial cells and in motor and bipolar neurons. On the contrary, negative Bcl-2 expression was noticed in the trauma + allopurinol group. Conclusions: This study is of importance to understand the effects of allopurinol in preventing degenerative changes in nerve and glial cells related to spinal cord injuries. (Folia Morphol 2019; 78, 4: 676–683)
2

Biochemical and immunohistochemical investigations on bone formation and remodelling in ovariectomised rats with tamoxifen citrate administration

100%
Baloglu M., Ozkorkmaz E. G.
Folia Morphologica
|
2019
|
tom 78
|
nr 4
Background: Osteoporosis results with the imbalance between osteoblastic formation and osteoclastic resorption, resulting in susceptibility to bone fractures. Ovariectomy leads to osteoporosis by triggering alterations in bone formation and structure. Tamoxifen as an anti-oestrogen is used for adjuvant therapy especially in metastatic diseases and known to have a bone mass protective effect after ovariectomy. Materials and methods: An animal model of ovariectomy induced osteoporosis after tamoxifen citrate administration was studied via biochemical and immunohistochemical methods. Female Wistar albino rats (n = 45), selected according to their oestrous cycle, were divided into three groups; I — control, II — ovariectomy, III — ovariectomy + tamoxifen. Following ovariectomy, tamoxifen citrate (10 mg/kg) was given intraperitoneally daily for 8 weeks. At the end of the period, animals were sacrificed under anaesthesia, blood samples were taken to measure oestrogen, calcium, and alkaline phosphate. Tibia bone samples were fixed in formalin solution and decalcified with 5% ethylene-diamine tetra acetic acid. After the routine histological follow up, samples were embedded in paraffin and cut with a microtome for semi-thin sections. Primary antibodies osteonectin and osteopontin were applied to sections and examined under light microscope. Results: As a consequence, when oestrogen and calcium data were compared there was a decrease in ovariectomy group with an increase in alkaline phosphatase. In ovariectomy + tamoxifen group, these values were close to the control group. Osteonectin was observed to promote bone formation by influencing collagen fibre formation, extracellular matrix development, osteoblast differentiation and the capacity to affect osteoclast activity. Conclusions: It has been suggested that osteopontin, the cytokine and cell binding protein, stimulates cellular signalling pathways, induces bone remodelling and acts in osteoporosis. (Folia Morphol 2019; 78; 4: 789–797)
3

Neuroprotective effects of Potentilla fulgens on spinal cord injury in rats: an immunohistochemical analysis

80%
Baloglu M., Cetin A., Tuncer M. C.
Folia Morphologica
|
2019
|
tom 78
|
nr 1
Background: This examination was performed to research the advantage of the antioxidant impact of Potentilla fulgens on spinal cord injury (SCI) in rats. Materials and methods: In the SCI model of this examination, the tolerably serious lesion was performed at the L1–L2 spinal segmental level. SCI animals were given P. fulgens 400 mg/kg/day, intraperitoneally. At 7 days post-lesion, exploratory rats were executed after intraperitoneal administration 7 ketamine HCL (0.15 mL/100 g body weight). Spinal cord specimens were taken for histological examination or assurance of malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) action. SCI caused a remarkable decline in spinal cord GSH content, trailed by noteworthy increments in MDA levels and MPO action. Results: Degenerative changes in some multipolar and bipolar nerve cells and pyknotic changes in the nuclei of glial cells were likewise noticed. Remarkable development was seen in cells and vascular structures of P. fulgens treated groups when contrasted with untreated groups. Conclusions: Potentilla fulgens application may influence angiogenetic improvement in vein endothelial cells, reduce inflammatory cell aggregation by influencing cytokine system and may make apoptotic nerve cells and neuroprotective component in glial cells. (Folia Morphol 2019; 78, 1: 17–23)
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