Abstract-Carbon tetrachloride (CC14) enhances lipid peroxidation, resulting in triglyceride accumulation in the liver. In this report, we studied the therapeutic, but not the preventive, effect of garlic extract on CC14-intoxicated liver, in comparison to the effect of vitamin E. Garlic extract was given orally to mice in the dose of 10, 100 or 500 mg/kg at 6 hr after CC14 administration.The increased conjugated diene level was diminished significantly to 82% by the 100 mg/kg extract, and also thiobarbituric acid-reactivity was inhibited by all the doses of the extract. In addition to the above mentioned effects, the high doses of garlic extract lowered hepatic triglyceride and lipid contents.Highly significant and positive correlation was observed between hepatic triglyceride content and conjugated-diene level in the lipid fraction of the liver. Besides, vitamin E at the dose of 25 mg/kg inhibited only lipid peroxidation.We, therefore, conclude that not only is garlic extract effective on diminution of lipid peroxide and on alteration of peroxidative status to more reductive condition like the effect of vitamin E, but it also inhibits hepatic triglyceride accumulation in injured liver.
Abstract-The effect of the combination of aminopyrine and secobarbital at a molar ratio of 2:1, the mixture and molecular compound, on rabbit EEG activation was examined. Secobarbital 40 mg/kg p.o. elevated threshold voltages in the neocortical and hippocampal EEG activation by high frequency electrical stimulation of the midbrain reticular formation (MRF), nucleous centralis medialis (CM) of the thalamus, and posterior hypothalamus (PHA) by 40, 40 and 80 %, respectively. Aminopyrine 80 mg/kg p.o. alone did not affect the arousal responses . The molecular compound 120 mg/kg p.o. has more potent and long-lasting actions in inhibiting the arousal responses induced by the stimulation of MRF (80%) and CM (50%) than with seco barbital alone. The inhibitory action of the mixture 120 mg/kg p.o. on the PHA arousal response (40 %) was significantly weaker than that of the molecular compound (80%). Secobarbital and the molecular compound slightly inhibited the neocortical augmenting and recruiting responses. Our findings suggest that although aminopyrine exerts a synergistic effect with secobarbital in inhibiting the EEG activation produced by MRF stimulation, in inhibiting the PHA-arousal response, there is no synergistic effect of the two drugs when they were given as the mixture. Moreover, the molecular compound rather than the mixture has a more potent inhibitory action on the EEG activation, particularly with PHA stimulation.Aminopyrine shows analgesic effects, although it has excitatory actions on the central nervous system (1). One of the barbiturates, secobarbital , is a short-acting hypnotic.The combination of the two drugs exhibits strong analgesic actions similarly to the combi nation of aminopyrine and barbital (2). In fact, we have unpublished data showing that when 2 molar aminopyrine and 1 molar secobarbital were simultaneously given p .o. as the mixture, they showed more potent analgesic effects than each of these drugs , and that the combination consisting of the molecular compound in which aminopyrine was linked by a hydrogen bond to secobarbital at the molar ratio of 1:1 and another 1 molar aminopyrine, exerted more potent analgesic actions than the mixture.A potentiation of analgesic action by the combination may be due to the finding that aminopyrine affects the absorption and metabolism of secobarbital (3, 4), resulting in high blood levels of these drugs. However, there is no precise electrophysiological analysis on
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