Antiinflammatory and acute toxicity studies with the leaves of Vinca rosea Linn in experimental animals.
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Biomedical subjects
Publications and source records attributed to R N Banerjee.
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Effect of A. indica leaf extract on serum enzyme levels (glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, acid phosphatase and alkaline phosphatase) elevated by paracetamol in rats was studied with a view to observe any possible hepatoprotective effect of this plant. It was interesting to observe that serum enzyme levels were much elevated in paracetamol induced animals than in those receiving a combination of paracetamol and lead extract. It is stipulated that the extract treated group was protected from hepatic cell damage caused by paracetamol induction. The findings were further confirmed by histopathological study of liver.
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Oral administration of water fraction of alcoholic extract of leaves of Vinca rosea (fam. apocynaeceae) led to marked lowering of blood glucose level in normal and streptozotocin induced diabetic rats. The hypoglycemic effect of the fraction was comparable with that of tolbutamide.
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Effects of phenformin on blood sugar, serum triglyceride, thrombin time, euglobulin clot lysis time and cardiovascular complications were studied in maturity onset diabetes and in atherosclerotic patients with or without diabetes, for a period of 14-18 months. Phenformin has shown the characteristic properties of an antifibrinopathic agent in that it prolongs thrombin time and enhances fibrinolysis. The hypoglycaemic effect of phenformin was found to be directly related to its antifibrinopathic action. Plasma lipids fell in all cases. Absence of fresh cardiovascular complications and improvement in anginal symptoms were observed. The metabolic, haematological and clinical benefits of phenformin and its limitations in maturity onset diabetes and atherosclerosis may be explained by the effects of the drug upon the thrombin-fibrinogen reaction. These results lend support to the hypothesis of a primary fibrinopathic pathogenesis in maturity onset diabetes mellitus and atherosclerosis.
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