Restoration of ultrastructural and biochemical changes in alloxan-induced diabetic rat sciatic nerve on treatment with Na3VO4 and Trigonella—a promising antidiabetic agent

Abstract

Vanadium has been reported to have broad pharmacological activity both in vitro and in vivo. Vanadium compound, sodium orthovanadate, Na3VO4, is well known for its hypoglycaemic effects. However, Na3VO4 exerts these effects at relatively high doses (0.6 mg/ml) and exhibit several toxic effects. In the present study lower doses of Na3VO4 (0.2 mg/ml) are combined with Trigonella foenum graecum seed powder (TSP), another hypoglycaemic agent, to reduce its toxicity without compromising its antidiabetic potential. The efficacy of the lower doses of Na3VO4 has been investigated in restoring the altered glucose metabolism and histological structure in the sciatic nerves in 21 and 60 days alloxan diabetic rats. A portion of the glucose was found to be channelled from the normal glycolytic route to polyol pathway, evident by the reduced hexokinase activity and increased polyol pathway enzymes aldose reductase and sorbitol dehydrogenase activity causing accumulation of sorbitol and fructose in diabetic conditions. Ultrastructural observation of the sciatic nerve showed extensive demylination and axonal loss after eight weeks of diabetes induction. Blood glucose levels increased in diabetic rats were normalized with the lower dose of vanadium and Trigonella treatment. The treatment of the diabetic rats with vanadium and Trigonella prevented the activation of the polyol pathway and sugar accumulations. The sciatic nerves were also protected against the structural abnormalities found in diabetes with Trigonella foenum graecum as well as Na3VO4. Results suggest that lower doses of Na3VO4 may be used in combination with TSP as an efficient antidiabetic agent to effectively control the long-term complications of diabetes in tissues like peripheral nerve.

Antidiabetic and Neuroprotective Effects of Trigonella Foenum-graecum Seed Powder in Diabetic Rat Brain

“…Hyperglycemia during diabetes has been shown to generate free radicals, increase damage to membranes and decrease antioxidant status (Kumar and Menon, 1993;Preet et al, 2005). Present results showed that three weeks treatment of the diabetic group with insulin, and TSP separately resulted in a marked reduction in hyperglycemia in the diabetic animals (Mohammad et al, 2006;Baquer et al, 2011;Kumar et al, 2011b, c).…”

“…Lipid peroxidation of the neuronal membrane causes loss of membrane fluidity and inhibition of membrane linked enzymes, increased neurolipofuscin deposition leading to diminished neurotransmitter uptake and loss of membrane asymmetry (Kamboj et al, 2009;Baquer et al, 2011). Previous studies from our laboratory have demonstrated that oral administration of Trigonella foenum-graecum seed powder to diabetic animals can lower blood glucose levels and partially restore the activities of key enzymes of carbohydrates and lipid metabolism to near normal levels in various animal models of diabetes (Raju et al, 2001;Preet et al, 2005;Mohammad et al, 2006;Baquer et al, 2011;Kumar et al, 2011b, c).…”

Antidiabetic and antioxidant activity ofSwietenia mahagoniin streptozotocin-induced diabetic rats

“…It plays an important role in detoxification and in the protection of cellular constituents against reactive oxygen species (Preet et al, 2005). Loven et al (1986) suggested that a decrease in hepatic GSH could be the result of decreased synthesis or increased degradation of GSH by oxidative stress in STZ-induced diabetes.…”

A metabolic and functional overview of brain aging linked to neurological disorders

“…Decrease in ROS scavenging compounds may be due to the direct affect of diabetes and aging on scavenger production or activity, like enhanced protein glycation may be responsible for the reduced enzymatic anti-oxidant activity of superoxide dismutase Mohamad et al 2004). Alteration of glutathione levels may be related to an increased polyol pathway (Preet et al 2005) activity as this leads to a depletion of NADPH which is necessary for the enzymatic reduction of oxidized glutathione (Fig. 2).…”