Rabbits hepatic disease

Ethanol has long been implicated in inducing toxic liver disease. Many studies have been concerned with ethanol s effect on hepatic protein synthesis. 1 Rothschild etal.108 reported that the addition of L-tryptophan to isolated perfused livers of rabbits treated with ethanol aided in the recovery of albumin synthesis. 

To summarize, based on the available data, pharmacological inhibition of ASMase might be an opportunity to prevent apoptosis, in particular in the liver, without influencing T-cell apoptosis. In fact, hepatocyte apoptosis is an important element in a number of liver diseases, ranging from cholestatic and alcoholic liver disease to autoimmune and viral hepatitis (Eichhorst, 2005). Furthermore, a role of ASMase-produced ceramide in neuronal and myocardial apoptosis has been implicated from studies in models of rat cerebral and rabbit heart ischemia, respectively (Yu et al., 2000 Argaud et al., 2004) the criticism to the latter two studies is, however, that their conclusion rely on the use of the xanthogenate D609, which inhibits ASMase in an indirect way but certainly is not specific for that enzyme. 

Documented effects In experiment on animals, this plant species had hypotensive, antispasmodic, anti-inflammatory, and styptic properties (Plant Resources of the USSR 1985). A methanol extract of the plant induced a dose-dependent relaxation of duodenal smooth muscle in rabbits (Atta and Mouneir 2004). Mice fed high doses of the plant died or had severe hepatic necrosis and gastritis after 4-7 days. Mice fed low doses of the plant had no clinical disease or large lesions, but developed mild multifocal hepatitis and gastritis (Schultheiss et al. 1995). 

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