deoxycholic-acid and Atrophy

Disruption of the blood-brain barrier (BBB) is a characteristic finding in common neurological disorders. Human data suggest BBB disruption may underlie cerebral dysfunction. Animal experiments show the development of epileptiform activity following BBB breakdown. In the present study we investigated the neurophysiological, structural and functional consequences of BBB disruption. Adult rats underwent focal BBB disruption in the rat sensory-motor cortex using the bile salt sodium deoxycholate (DOC). Magnetic resonance imaging in-vivo showed an early BBB disruption with delayed reduction in cortical volume. This was associated with a reduced number of neurons and an increased number of astrocytes. In-vitro experiments showed that the threshold for spreading depression and the propagation velocity of the evoked epileptic potentials were increased 1 month after treatment. Furthermore, animals' motor functions deteriorated during the first few weeks following BBB disruption. Treatment with serum albumin resulted in a similar cell loss confirming that the effect of DOC was due to opening of the BBB. Our findings suggest that delayed neurodegeneration and functional impairment occur following the development of the epileptic focus in the BBB-permeable cerebral cortex.

Topics: Animals; Astrocytes; Atrophy; Blood-Brain Barrier; Cerebral Arteries; Cerebrovascular Circulation; Cortical Spreading Depression; Deoxycholic Acid; Dyskinesia, Drug-Induced; Epilepsy; Gliosis; Magnetic Resonance Imaging; Male; Neocortex; Nerve Degeneration; Neural Conduction; Organ Culture Techniques; Rats; Rats, Wistar; Serum Albumin; Time Factors

To establish an experimental animal model of chronic gastritis in a short term and to investigate the effects of several potential inflammation-inducing factors on rat gastric mucosa.. Twenty-four healthy, male SD rats were treated with intragastric administration of 600 mL/L alcohol, 20 mmol/L sodium deoxycholate and 0.5 g/L ammonia (factor A), forage containing low levels of vitamins (factor B), and/or indomethacin (factor C), according to an L(8) (2(7)) orthogonal design. After 12 wk, gastric antral and body mucosae were pathologically examined.. Chronic gastritis model was successfully induced in rats treated with factor A for 12 wk. After the treatment of animals, the gastric mucosal inflammation was significantly different from that in controls, and the number of pyloric glands at antrum and parietal cells at body were obviously reduced (P<0.01). Indomethacin induced gastritis but without atrophy, and short-term vitamin deficiency failed to induce chronic gastritis and gastric atrophy. In addition, indomethacin and vitamin deficiency had no synergistic effect in inducing gastritis with the factor A. No atypical hyperplasia and intestinal metaplasia in the gastric antrum and body were observed in all rats studied.. Combined intragastric administration of 600 mL/L alcohol, 20 mmol/L sodium deoxycholate and 0.5 g/L ammonia induces chronic gastritis and gastric atrophy in rats. Indomethacin induces chronic gastritis only. The long-term roles of these factors in gastric inflammation and carcinogenesis need to be further elucidated.

Topics: Alcohols; Ammonia; Animals; Anti-Inflammatory Agents, Non-Steroidal; Atrophy; Chronic Disease; Deoxycholic Acid; Disease Models, Animal; Gastric Mucosa; Gastritis; Indomethacin; Male; Rats; Rats, Sprague-Dawley; Vitamins

To establish a rat model of chronic atrophic gastritis and explore the factors inducing atrophy.. In accordance with repeated orthogonal design of L8(2(7)), 60% alcohol and 20 mmol/L sodium deoxycholate (served as factor A), 0.05%-0.1% ammonia water (factor B), 0.05% indomethacin (factor C) were given, alone or in combination, to rats in three experiments for 3 months, 6 months or 9 months respectively. Then the rats were dissected, and their pathologic changes of the gastric mucosa were assessed.. Typical signs of chronic atrophic gastritis (CAG) were found in all rats which were treated with factor A, B, C alone or in combination for 6 or 9 months. No significant difference of pathologic changes of gastric mucosa was found between the rats treated for 6 months and those for 9 months. No obvious CAG signs were found in the rats treated with factor A, B, C for 3 months.. Sixty percent of alcohol, 20 mmol/L sodium deoxycholate, 0.05%-0.1% ammonia water and 0.05% indomethacin given to Sprague-Dawley rats for 6 months can successfully establish the animal model of CAG. Prolongation of the model-establishment time is not able to further facilitate the atrophy of gastric mucosa.

Topics: Ammonia; Animals; Atrophy; Deoxycholic Acid; Disease Models, Animal; Ethanol; Gastric Mucosa; Gastritis, Atrophic; Indomethacin; Male; Rats; Rats, Sprague-Dawley; Time Factors