Objective: This study reports protective effect of Abelmoschus moschatus seed extract against sodium fluoride-induced neurodegeneration through oxidative stress, neurohistological, and behavioral observations in Wistar rats.Methods: A total of 20 Wistar rats (around 250 g) were randomly classified into four groups, namely, control, fluoride (NaF), fluoride + A. moschatus seed aqueous extract (AMAE), and fluoride + A. moschatus seed ethanol extract (AMEE). The control group animals received normal tap water, fluoride group received fluoridated water at the rate of 40 mg/kg b. wt., 3rd group rats treated with fluoride (40 mg/kg b. wt.) + AMAE (300 mg/kg b. wt.), and 4th group rats treated with fluoride (40 mg/kg b. wt.) + AMEE (300 mg/kg b. wt.). Neurobehavioral responses of rotarod, hot plate, and maze learning tests and oxidantive stress markers including lipid peroxidation (LPO), GSH levels, superoxide dismutase, CAT, and GSH peroxidase (GPx) activities, and also histology with H and E as well as congo red staining were studied in control, fluoride, and A. moschatus seed extract treated against fluoride groups.Results: Decreased neurobehavioral responses with rotarod, hot plate, and maze and enhanced LPO (p<0.05) levels were found in fluoride received animals. Whereas, the superoxide dismutase (SOD), CAT, GSH, and GPx were decreased (p<0.05) in NaF treatment. The rats received seed extract along with NaF showed significant reversal of behavioral and oxidative stress markers and the effect of ethanol extract was more pronounced than aqueous extract. The fluoride-treated group showed disturbed cell structure and reduced number of cells in H and E as well as congo red staining which was reversed in cell morphology and restored cell number in seed extract against NaF-treated group. As a result of increased LPO, decreased antioxidant system, and decreased number of cells, neurodegeneration was observed resulting in the disturbance in functions associated with reported behavior.Conclusion: Okra with high antioxidants activity, seed extract showed reversal of LPO levels and antioxidant status in the brain tissue. And also plant extract administered rats displayed normal cell structure and number of cells than only fluoride received group. Therefore, the aqueous and ethanolic extract of A. moschatus plant seeds has neuroprotective effects against fluoride-induced motor, nociceptive, learning behavior, and on histological structure of brain through antioxidant mechanism. The ethanol extract has shown more efficacy than aqueous extract.

Coccinia grandis has been used in tribal populations of India both as food and medicine, but it has been not reported to be a neuroprotective agent yet. The present study was designed to evaluate the protective effects of Coccinia grandis leaf extract on diabetes induced brain damage of Wistar rats. This study reports the protective effect of methanolic leaf extract of Coccinia grandis against STZ induced diabetes in rats. Metformin (150mg/kg body wt.) was used as a reference drug. The enzymes of the polyol pathway and its related substrates were studied in the brain tissue. The effect of Coccinia on Cyclooxygenase (COX) and Prostaglandin peroxidise (PG) was also studied. Diabetes induced rats showed a significantly increased activity of Aldose reductase, Sorbitol dehydrogenase, Glucose-6-phosphodehydrogenase, whereas the decreased activity of Hexokinase. The content of Glucose, Sorbitol significantly increased in rat brain. Sodium potassium ATPase activity was also decreased in diabetic rats. COX, PG peroxidase was increased. Histological alternations were induced in the hippocampus of STZ treated diabetic rats. Oral administration of Coccinia leaf extract (200mg/kg) of body weight to diabetic rats for 21 days efficiently attenuated the parameters studied. A decreased activity of brain AR, sorbitol dehydrogenase, glucose-6-dehydrogenase was observed along with the increase in Hexokinase and Sodium potassium ATPase activity. It also showed decreased content of glucose and Sorbitol. Diabetes induced brain damage in the hippocampus and cerebral cortex was restored with Coccinia treatment. Decreased COX and PG peroxidase suggest its protection against inflammation. The current results suggest that Coccinia grandis leaf extract exerts the potential ability to reverse the progression of hyperglycemia and its concomitant induced brain damage.

Fluoride is one of the common environmental pollutants. Its excessive exposure results in a wide array of toxicity phenotypes including oxidative stress, skeletal and soft tissue damage etc. Antioxidants such as Selenium (Se) and α-tocopherol are attractive agents for oxidative stress prevention because of their safety profile and wide availability. It is known that in combination, Se and alpha-tocopherol act synergistically against ROS formation. This study investigated the protective effects of selenium (05 µg/kg BW) and Alpha-tocopherol (2 mg/kg BW) on markers of oxidative stress in brain and muscle of mice exposed to sodium fluoride (20mg/kg BW) for 15 days. The results showed significant (p<0.05) alterations in markers of oxidative stress includes; an increase in xanthine oxidase activity and lipid peroxidation, a decline in SOD, CAT, GST and GPx activities in fluoride exposure group in comparison with control group indicates oxidative stress induced by fluoride. These changes were reversed modestly in Se and alpha-tocopherol alone treated groups and significantly  (p<0.05) in the combinedly treated group indicating synergistic action in mitigation of fluoride effect.

The aim of the present study was to evaluate the protective effect of methanol garlic extract on the enzymes related with polyol pathway, advanced glycation end products, markers of oxidative stress and antioxidant status in brain of streptozotocin induced diabetic rats. Antioxidant capability of methanol extract of garlic was evaluated by 2,2-diphenyl-2-picrylhydrazyl hydrate radical and FOX (ferrous ion oxidation-xylenol orange) H2O2 scavenging test. Diabetes was induced by single i.p injection of STZ (32mg/kg per body Wt.,). Blood glucose levels and body wt, were measured on every 7th day over a period of 30 days. The diabetic rats treated with garlic extract at two doses 250mg/kg and 500mg/kg body wt., by oral administration. Diabetic rats showed significant increase in food and water intake, decrease in blood glucose levels, body weights, but could not show any recovery by garlic treatment. Garlic treatment significantly decreased aldose reductase (AR); sorbitol dehydrogenase (SD) and glutathione S-transferase (GST) enzyme activities. A decrease of malndialdehyde (MDA), Protein carbonyls (PC), Pentosidine advance oxidation protein products (AOPP), Advanced glycation end products (AGEs) was also observed. Additionally garlic administration produced a restoration of brain superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and reduced glutathione (GSH) in diabetic rats. Garlic treatment also reduced the free radical formation and progression of hyperglycemia induced diabetic complications by decreasing influx of glucose into the polyol pathway and increased activity of antioxidant enzymes. The current study reveals exerts, efficiently, an attenuating effect of methanol garlic extract exterted antihyperlgycemic, antioxidant and anti-glycating effects in a dose dependent manner in diabetic rats.