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Changes in glucocorticoid-induced apoptosis and in expression of Bcl-2 protein during long-term culture of thymic lymphoma

100%

Kobzdej M. , Matuszyk J. , Ziolo E. , Strzada?a L. , Strzada?a L.

Archivum Immunologiae et Therapiae Experimentalis

2000

tom 48

nr 1

43-46

Lymphomagenesis is a multistep process progressively freeing transformed thymocytes from external regulatory signals, i. e. thymic developmental program controlling growth, differentiation or apoptosis. Here we report that cells of thymic lymphoma overexpressing Ras/Raf proteins, initially resistant to TCR-dependent apoptosis but sensitive to dexamethasone- and etoposide-induced cell death, became insensitive to dexamethasone after long-time culture. That transition correlated with a strong increase in the expression of the anti-apoptotic Bcl-2 protein. Interestingly, lymphoma cells were still sensitive to p53-mediated apoptosis induced by etoposide. It suggests that the anti-apoptotic activity of Bcl-2 is correlated with a resistance to glucocorticoid-induced apoptosis but not to p53-mediated apoptosis. The sequence of mutations in the process of lymphomagenesis seems to be composed of at least 3 main hits which equip the cells with independence from external mitogenic signals (activation of Ras/Raf), resistance to inducers of apoptosis (activation of Bcl-2) and generation of cellular heterogeneity (deletion of p53) important in tumor progression.

Adrenal steroids act as inhibitory modulators of thyrofollicular cell morphology and proliferation in neonatal chicks (Gallus domesticus)

88%

Ganguli S. , Bandyopadhyay R. , Chakraborty S.

Folia Biologica

2001

tom 49

nr 3-4

259-263

In the present study the effects of adrenal corticoids, both natural and synthetic, namely cortisol and dexamethasone respectively, was observed on the thyroid gland cell morphology and proliferation in neonatal male chicks (Gallus domesticus). Cortisol was injected at a dose of 4 mg/100 g body weight and dexamethasone at a dose of 1 mg/100 g b.w. subcutaneously daily for fifteen consecutive days. The control birds were similarly injected with normal saline at a daily dose of 0.2 ml per bird for the same time period. The results indicated that both cortisol and dexamethasone caused a significant decrease in thyrofollicular cell height. On the contrary, a significant increase in the ratio of the follicular diameter to the number of nuclei per follicle i.e. D/N value was observed in both cortisol and dexamethasone treated chicks. It was also observed that both cortisol and dexamethasone induced suppression of mitotic activity, as evidenced from a significant decrease in mitotic percentage compared with the control chicks. The present authors? studies thus indicate that adrenal corticoids act as inhibitory modulators of thyroid follicular activity as regards karyomorphology and cell proliferation.

Neuroprotective effect of ACTH (4-9) in degeneration of hippocampal nerve cells caused by dexamethasone: morphological, immunocytochemical and ultrastructural studies

75%

Sekita-Krzak J. , Zebrowska-Lupina I. , Czerny K. , Stepniewska M. , Wrobel A.

Acta Neurobiologiae Experimentalis

2003

tom 63

nr 1

1-8

. Sustained exposure to glucocorticosteroids (GCs), adrenal hormones secreted during stress, can cause neural degeneration. This is particularly so in the hippocampus, a principal neural target site for GCs. The purpose of this research was an assessment of the neuroprotective effect of ACTH (4-9) in degenerative changes of hippocampal neurons induced by synthetic GC - dexamethasone. Experiments were conducted on male Albino-Swiss mice. We studied the morphology of neurons in the dorsal hippocampus in slides stained with cresyl violet. Immunocytochemical analysis was carried out with the use of monoclonal antibody anti-MAP2 in order to detect alterations in the the neuronal cytoskeleton. We also performed ultrastructural examinations of hippocampal neurons. Quantitative analysis of morphological changes was completed using a computer analyser of histological pictures. It was shown that dexamethasone administered in toxic doses evokes neuronal death in layer CA3 of the hippocampus. Results indicate that ACTH (4-9) shows protective effects in that model. Dexamethasone-induced damage to hippocampal pyramidal neurons (assessed by cell counts, immunocytochemical analysis of cytoskeletal alterations and ultrastructural studies) was significantly reduced in animals administered ACTH (4-9).