Hepatic encephalotathy in swine experimentally poisoned with Senna occidentalis seeds: Effects on astrocytes

Abstract

Senna occidentalis may be accidently ingested by humans and animals. In this study, the percentages of S. occidentalis seeds necessary for experimental reproduction of hepatic encephalopathy were determined in a pig model and the biochemical and microscopic pathology is described in detail, with emphasis on the astrocytes. The experimental groups (G1, G2 and G3) were fed rations containing 5%, 7.5% and 10% of S. occidentalis seeds for 7–11 days. Pigs from the three experimental groups showed incoordination, ataxia, disorientation, head pressing, anorexia, recumbency and depression. In addition, the enzymes aspartate aminotransferase, alkaline phosphatase and creatine phosphokinase increased in all treated animals, which also showed higher serum total bilirubin and ammonia levels than in the control group (C). Microscopically, all experimental animals revealed acute hepatocellular swelling, multifocal coagulative necrosis in the pancreas, necrosis in the cardiac muscle, severe spongiosis in brain white and grey matter, and Alzheimer type II astrocytes in grey matter of the cerebral cortex. These cells were glial fibrillary acidic protein (GFAP) negative in G3. In white matter, a decrease in the positive area occupied by GFAP-immunolabelling and in the number of astrocytes per immunoreactive area was observed in G3 animals (5.35 ± 1.14% and 410 ± 45 cells/mm2, respectively) compared to the C animals (13.93 ± 1.59% and 581 ± 36 cells/mm2, respectively). This loss of GFAP was accompanied by alterations in astrocyte morphology, such as shrinkage of the cell body and retraction of the extending processes. This pig model of ammonia-mediated astrocyte damage could be used to study not only poisoning by S. occidentalis, but also other medical conditions resulting in hepatoencephalopathy.