Hypoglycaemiant and anti-hyperglycaemiant effect of juscticia secunda m. vahl (acanthaceae) on glycaemia in the wistar rat
International Journal of Development Research
Hypoglycaemiant and anti-hyperglycaemiant effect of juscticia secunda m. vahl (acanthaceae) on glycaemia in the wistar rat
Received 30th March, 2017; Received in revised form 29th April, 2017; Accepted 07th May, 2017; Published online 20th June, 2017
Copyright© 2017, Mea et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
In animal experiments, it is possible to induce hyperglycaemia in healthy animals. Subsequently, the administration of drugs makes it possible to measure the evolution of this hyperglycaemia induced. It is this pharmacological method that we used in this work to evaluate the effect of Justicia secunda on healthy animals and made hyperglycaemic. The basal glucose levels ranged from 0.59 ± 0.02 g / l to 1.2 ± 0.05 g / l in fasted rats used in these different experiments. From 2 to 3 g / kg BW, AEJs induces dose-dependent hypoglycemia in normoglycaemic rats. The glucose administration of 4 g / kg BW (by force-feeding) of anhydrous glucose induced hyperglycaemia (glucose > 1.2 ± 0.05 g / l) which was measurable. Thus, a peak increase in blood glucose occurs 30 minutes after treatment. The hyperglycemia thus induced by glucose is progressively reduced and canceled in the animals treated with EAJs and glibenclamide. When the rats were pretreated (treated before force-feeding with glucose) with AEJs at doses of 2.5 g / kg BW and 3 g / kg BW on the one hand and glibenclamide at 10-2 g / kg BW, on the other hand, the glucose-induced hyperglycemia peak is lower than that of the non-pretreated hyperglycaemic control. The reduction in hyperglycaemia is more pronounced. The cancellation of this hyperglycaemia occurs more rapidly. Similarly, in post-treated animals, the return of blood glucose to normal is faster compared to hyperglycemic control rats. After return to basal glucose, hypoglycemia was observed at high doses of AEJs and glibenclamide. The dose reduction of glucose-induced hyperglycemia was dose-dependent and the dose of 3 g / kg BW was substantially identical (P> 0.05) to that of glibenclamide at 10-2 g / kg BW. Examination of the liver-released glucose level of control normoglycemic rats and normoglycemic rats treated with AEJs and glibenclamide shows that AEJs and glibenclamide decrease the glucose released by the liver.
