European review for medical and pharmacological sciences · 2012
Antihyperglycemic and protective effects of Trigonella foenum graecum seed powder on biochemical alterations in alloxan diabetic rats.
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Kumar P, Kale R K, Baquer N Z
Аннотация
BACKGROUND: Trigonella foenum-graecum, an annual herb belonging to the family Leguminosae, commonly known as fenugreek, has been reported to have hypoglycemic, hypocholesterolemic, hyperinsulinemic and antidiabetic properties. In the present study, the effect of oral feeding of Trigonella foenum-graecum seed powder (TSP) has been studied on blood glucose, monoamine oxidase (MAO), membrane fluidity, neurolipofuscin content, DNA degradation and glucose transporter-4 (GLUT4) accumulation in the alloxan-induced diabetic rat brain.
METHODS: Diabetes was induced by administration of alloxan monohydrate (15 mg/100 g body weight) and diabetic rats were treated with 2 IU insulin, per day and 5% TSP in the diet for 21 days.
RESULTS: Diabetic rats showed hyperglycemia with almost four fold high blood glucose levels. Increased MAO activity with correlated increase in genomic DNA degradation in the diabetic brain supports the hypothesis that catecholamine oxidation is an important source of oxidative stress, causing loss of membrane fluidity, increased neurolipofuscin and decreased of GLUT4 expression with diabetes in the brain. The present study showed that TSP treatment reversal the changes to near normal levels in diabetic rat brain.
CONCLUSIONS: The present findings indicate that the TSP exerts its anti-diabetic and neuroprotective effects, probably mediated through a decrease in hyperglycemia and oxidative stress thereby ameliorating the control and management of diabetic complications.
METHODS: Diabetes was induced by administration of alloxan monohydrate (15 mg/100 g body weight) and diabetic rats were treated with 2 IU insulin, per day and 5% TSP in the diet for 21 days.
RESULTS: Diabetic rats showed hyperglycemia with almost four fold high blood glucose levels. Increased MAO activity with correlated increase in genomic DNA degradation in the diabetic brain supports the hypothesis that catecholamine oxidation is an important source of oxidative stress, causing loss of membrane fluidity, increased neurolipofuscin and decreased of GLUT4 expression with diabetes in the brain. The present study showed that TSP treatment reversal the changes to near normal levels in diabetic rat brain.
CONCLUSIONS: The present findings indicate that the TSP exerts its anti-diabetic and neuroprotective effects, probably mediated through a decrease in hyperglycemia and oxidative stress thereby ameliorating the control and management of diabetic complications.