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Choline acetyltransferase activity in selected rat tissues following experimental diabetes and treatment with panax ginseng extract
Journal of the Egyptian Society of Toxicology. 2007; 37: 107-118
en Inglés | IMEMR | ID: emr-83728
ABSTRACT
The activity of the acetylcholine synthesizing enzyme, choline acetyltransferase [ChAT] in seven brain regions, heart, liver and serum of adult male albino rat was determined following diabetes induction by a single subcutaneous injection of alloxan monohydrafe, oral administration of Panax ginseng extract for 12 consecutive days and the co-administration of both treatments. The changes in the enzyme activity of the selected tissues were estimated after 2, 4, 8 and 12 days of alloxan and/or Panax ginseng administration. The induction of diabetes was associated with a marked increase in the ChAT of the hypothalamus, midbrain and cerebellum at all the time intervals examined, a less pronounced increase in the cerebral cortex and thalamus and a decrease in pons and medulla, A tendency towards a decreased ChAT activity in the heart, significant fluctuations in liver and nonsignificant changes in serum were also noticed. However, administration of ginseng extract alone or following alloxan injection revealed enhanced ChAT activities in the different brain regions and nonsignificant decreases in liver and serum. It was concluded that the changes in the ChAT activity and the consequent alteration in the concentration of the cholinergic ncurotransmitter may be the mechanism by which the organism copes with the crisis of hyperglycemia and that ginseng extract may have beneficial effects at improving cholinergic function beside organ-protective functions
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Índice: IMEMR (Mediterraneo Oriental) Asunto principal: Tejidos / Diabetes Mellitus Experimental / Panax Límite: Animales Idioma: Inglés Revista: J. Egypt. Soc. Toxicol. Año: 2007

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Índice: IMEMR (Mediterraneo Oriental) Asunto principal: Tejidos / Diabetes Mellitus Experimental / Panax Límite: Animales Idioma: Inglés Revista: J. Egypt. Soc. Toxicol. Año: 2007