Vasant Kusumakar Rasa Ameliorates Diabetic Encephalopathy by Reducing Oxidative Stress and Neuroinflammation and Improving Neurotransmitter Levels in Experimental Animals.

PURPOSE

Diabetic encephalopathy (DE) is one of the complications of diabetes that affects the brain. In the Ayurveda system of medicine, Vasant Kusumakar Rasa (VKR) is cited as a classical herbo-mineral formulation for diabetes. However, the role of VKR in DE is still unclear.

METHODS

High-fat diet and streptozotocin (35 mg/kg, ) were used to induce type 2 DE in Sprague Dawley rats. VKR at doses 28 mg/kg and 56 mg/kg was given via intragastric route to diabetic rats for 16 weeks. Estimation of plasma glucose, serum insulin, glycohemoglobin, and C-reactive protein (C-RP) was analyzed. Furthermore, the Morris water maze test was performed to assess cognitive behavior. Pro-inflammatory, such as TNF-α, IL-1β, and IL-6, were measured in brain tissue homogenate. Antioxidant enzyme assays were performed to estimate the levels of malondialdehyde, reduced glutathione, superoxide dismutase, and catalase in brain tissue. Histopathology of brain sections was performed using hematoxylin and eosin (H & E) staining. Neurotransmitters (viz., serotonin (5-HT), dopamine (DA), and norepinephrine (NE)) were estimated in the brain by high-performance liquid chromatography (HPLC). The data were analyzed by using ANOVA, followed by Dunnett's multiple comparison test.

RESULTS

VKR treatment, at a dose of 28 and 56 mg/kg, reduced the plasma glucose level significantly (236.7±17.08 and 221.8±17.50, respectively; p<0.001) when compared with diabetic control (461.7±13.03). The treatment also reduced serum insulin and glycated hemoglobin levels and improved the escape latency in VKR-treated animals as compared to diabetic animals. Brain tissue pro-inflammatory marker levels were reduced, and oxidative stress enzymes showed positive marks in diabetic rats treated with VKR. Histopathology of the brain demonstrated a reduction in neuronal damage in the VKR-treated diabetic animals. VKR treatment at doses of 28 and 56 mg/kg also improved the levels of 5-HT (1.78±0.11 and 1.72±0.18, respectively) when compared with diabetic control (0.91±0.08) significantly (p<0.01). DA levels were significantly (p<0.01) increased in VKR-treated animals when compared with diabetic animals. The treatment of VKR for 16 weeks also improved the NE levels significantly when compared with diabetic control animals.

CONCLUSION

The result of the study indicates that the treatment with VKR for 16 weeks has significant therapeutic potential in the management of type 2 DE.