The above study justifies diosgenin as a promising candidate in diabetes associated complication through its antioxidant and anti-inflammatory activity.

Epilepsy is a brain disorder characterized by sudden recurrent seizures. Considering the fact that epileptogenesis is a process that affects the quality of life, our goal is to delay the process of epileptogenesis and to increase the latency of epileptic attacks, offering better quality of life to patients. Traditional system of medicines has a promise in some of the medicines, which have been used for the treatment of epilepsy. One such medicinal plant is Eclipta alba (EA). According to Ayurvedic philosophy, the juice of leaves of EA is pounded with garlic and pepper for the treatment of epilepsy. Taking clue from the Ayurvedic system of medicines, we formulated coumarin fraction of EA, namely, coumarin nasal formulation (CNF) for its nasal delivery. CNF was analyzed by using high performance liquid chromatography (HPLC) and ultraviolet absorption spectroscopy for its drug content determination. In vitro drug release studies were performed in simulated nasal electrolyte solution (SNES) maintaining constant pH of 5.5 at 37°C. Irritation by CNF was evaluated using hen’s egg test chorioallantoic membrane (HET-CAM) assay. Formulation was found to be non-irritant in HET-CAM assay. CNF was further assessed in vivo by measuring the progress and attainment of pentylenetetrazole (PTZ) kindling in mice. Neuronal changes were assessed by hematoxylin and eosin (H&E) and Nissl staining technique. Glial fibrillary acidic protein (GFAP) a neuroinflammatory marker and tumor necrosis factor alpha (TNF-α) an inflammatory marker were also measured. CNF (10 mg/kg, nasal route) when given as a pretreatment lowered seizure score and delayed the progression of seizure similar to diazepam. CNF decreased the PTZ induced oxidative damage, TNF-α as well as GFAP levels in the midbrain tissue particularly in hippocampus region. The results suggest that CNF may be a promising therapeutic approach to offer protection from sudden recurrent seizures alone or in combination with current drugs in management of epilepsy.

Background Diabetic retinopathy is a slow progressing complication of diabetes mellitus with multifactorial aetiology affecting approximately 80% of diabetics worldwide. Chronic hyperglycemic milieu of Diabetes induces biochemical changes which contribute to the pathogenesis of Diabetic retinopathy. Objective The present study examined the protective effect of Vasant Kusumakar Ras , an Ayurvedic herbo-mineral formulation, in diabetic retinopathy. Materials and Methods Diabetes was induced in rats by intraperitoneal injection of streptozotocin (45 mg/kg). Rats were kept without any treatment for period of three weeks for induction of Diabetic retinopathy followed by treatment with Vasant Kusumakar Ras (11.25 mg/kg, p.o) for further 5 weeks. Fasting blood glucose levels, lipid profile and HbA1c were determined. Eye tissue homogenates were subjected to biochemical analysis to determine the levels of oxidative stress parameters (superoxide dismutase, catalase, reduced glutathione, lipid peroxidation), vascular endothelial growth factor and aldose reductase activity. Histopathological analysis of retinal tissue was conducted using Hematoxylin and Eosin staining. Results Vasant Kusumakar Ras treatment restored serum lipid profile which was altered in diabetic rats. Treatment with Vasant Kusumakar Ras significantly ameliorated the oxidative stress in eye tissue resulting in decreased lipid peroxidation and increase in endogenous antioxidant levels. Levels of aldose reductase and vascular endothelial growth factor in eye tissue were significantly decreased in Vasant Kusumakar Ras treated rats. Hematoxylin and Eosin staining indicated that the Vasant Kusumakar Ras treatment significantly restored the normal architecture of the retinal tissue. Conclusion Vasant Kusumakar Ras exhibits protective effect and prevents the development of Diabetic retinopathy through its effects on multiple biochemical pathways implicated in pathogenesis of Diabetic retinopathy.

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