Histological examination of the liver after experimental administration of MK-801 and dexamethasone.

The aim of the research was histological assessment of the influence of MK-801 (NMDA receptor antagonist) and dexamethasone on the liver. The experiment was carried out on adult Albino-Swiss mouse males. MK-801 was administered in the dose of 0.3 mg/kg/24 h for 8 days, dexamethasone--in the toxic dose of 120 mg/kg/24 h. Liver slices stained with hematoxylin and eosin were examined with light microscope. The performed experiments revealed that MK-801 can cause morphological changes of the liver in the shape of increased transparence of hepatocyte cytoplasm and narrowing of the liver sinusoids. MK-801 intensifies liver damage induced by toxic doses of dexamethasone leading to focal necrosis of hepatocytes.

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

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 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).

Histological changes in neurons of the globus pallidus after experimental administration of dexamethasone.

The aim of our research was morphological assessment of neurons in the globus pallidus after 28-day administration of dexamethasone. The experiments were carried out on adult Albino Swiss mice males. It was found that prolonged administration of this glucocorticosteroid causes degenerative changes in neurons of the globus pallidus (shrinkage of nerve cells, increased stainability of nucleus and cytoplasm). We also observed increased numbers of glial cells in this area of the brain.

Protective effects of ACTH (4-9) in degeneration of hippocampal nerve cells caused by dexamethasone: ultrastructural studies.

The purpose of this research was an assessment of protective action of ACTH (4-9) in dexamethasone-induced neurodegeneneration on the base of ultrastructural examinations of hippocampal neurons in the CA3 region. The experiments were carried out on adult Albino Swiss mouse males. The animals were divided into three groups: control group, experimental group 1-dexamethasone 8 mg/kg/24 h for 28 days, experimental group 2-dexamethasone and ACTH (4-9) 50 micrograms/kg twice a week. Results of our investigations show that ACTH (4-9) prevents neurotoxic influence of dexamethasone and its protective action is connected with the ability to inhibit degenerative processes in neurons having a character of apoptosis.

Immunocytochemical examinations of hippocampal nerve cells after experimental administration of dexamethasone.

The purpose of this research was an assessment of MAP2 immunoreactivity in hippocampal neurons after administration of toxic doses of dexamethasone. Experiments were led on Albino-Swiss mouse males. The obtained results indicate that dexamethasone causes significant decrease of MAP2 immunoreactivity in hippocampal nerve cells of the CA3 region. Our results show damage of neuronal cytoskeleton in this area of the brain.

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

The purpose of this research was an assessment of neuroprotective effect of ACTH (4-9) in degenerative changes of nerve cells induced by dexamethasone. Experiments were led on Albino-Swiss mouse males. We examine morphological changes of neurons in the dorsal hippocampus in slides stained with cresyl violet and we performed quantitative analysis of neurodegenerative changes using a computer analyser of histological pictures. Achieved results indicate that ACTH (4-9) shows neuroprotective effect against neurotoxic influence of dexamethasone. This chemical inhibits dexamethasone induced degeneration of hippocampal nerve cells having morphological features characteristic of apoptosis.

The influence of Atorvastatin on ultrastructure of rat pancreatic exocrine cells in the course of experimental intoxication with ethanol.

The experiment was carried out on mature Wistar male rats. The animals from experimental group I received Atorvastatin in the dose 0.28 mg/24 h for 3 weeks. Experimental group II received 20% ethanol ad libitum apart from Atorvastatin. Ultrastructural examinations of pancreatic exocrine cells showed the stimulation of secretory processes in cells of animals receiving Atorvastatin and considerable damage of cell organelles in experimental group II, more intense than in the pancreas of control animals which drank ethanol.