The present study investigated the protective effect of curcumin and mitochondrial‐targeted curcumin (MTC) in rotenone‐induced cerebellar toxicity in mice. Treatment of rotenone in mice significantly shortened the stride length for both forelimb and hind‐limb and increased fore‐paws and hind‐limb base width. Co‐treatment of curcumin and MTC with rotenone improved the walking pattern. A significant increase in lipid peroxidation, nitric oxide and decreased activity of AChE, reduced glutathione, superoxide dismutase and catalase were observed in rotenone‐treated mice while co‐treatment of curcumin and MTC with rotenone significantly increased AChE activity and protected against rotenone‐induced oxidative damage. Rotenone exposed mice showed irregular, damaged Purkinje cells and perineuronal vacuolation while co‐treatment of curcumin and MTC with rotenone protected against rotenone‐induced cellular damage in these cells. The result exhibits that both curcumin and MTC showed protective effects against rotenone‐induced cerebellar toxicity in mice and MTC is more effective than curcumin.
Various studies suggested that neuroinflammation leads to the development of several neurodegenerative disorders like Parkinson's disease (PD), Alzheimer's disease (AD), and Huntington's disease (HD). Rotenone is an organic pesticide and potent inhibitor of complex I of electron transport chain widely used to develop the PD model. Numerous studies reported rotenone toxicity in the dopaminergic system but very few studies are available on rotenone‐induced glial cell activation and subsequent neurodegeneration and alterations in various types of behavior. Therefore, the present study was designed to explore the effect of rotenone on neuroinflammation and its deleterious effect on the behavior of mice, and also how these effects can be protected through quercetin. Quercetin, a natural flavonoid having strong antioxidant and anti‐inflammatory properties, is found in vegetables and fruits. The finding of the study indicated that rotenone 5 mg/kg body weight for 60 days through oral gavage leads to the release of inflammatory markers in blood serum, astrocytes activation in substantia nigra and hippocampus, and subsequently decreased density of dopaminergic fibers in the striatum. Rotenone also altered the memory of the mice as indicated by decreased spontaneous alteration in Y‐maze and T‐maze tests and reduction in exploration time in novel object recognition, increased immobility time in the forced swim test and reduced muscular strength. Co‐treatment of quercetin 30 mg/kg/day through oral gavage for 60 days along with rotenone significantly reversed all these adverse effects, suggesting that quercetin could reduce neuroinflammation, and improve memory, and cognitive function.
Rotenone is well known environmental neurotoxin used to induce Parkinson’s disease (PD) model. Numerous studies are investigated its toxicity on the brain but few studies are available that examined its toxicity on the liver and kidney. Therefore, the main aim of the present work was to explore the toxicity of rotenone on the liver and kidney and its protection through quercetin. Administration of rotenone orally at the dose of (5mg/kg b.w daily for 60 days) caused a significant increase in the levels of liver function and renal function biomarkers as compared to controls. A significant increase in the level of lipid peroxidation, nitric oxide, and decrease in the levels of reduced glutathione, reduction in the activities of catalase and superoxide dismutase were observed in the liver and kidney as compared to control. The histopathological and SEM study in rotenone-treated mice showed alteration and signs of inflammation in the liver and kidney. While co-treatment of quercetin orally (30 mg/kg b.w for 60 days) together with rotenone, reversed the above parameters. In conclusion, rotenone significantly damages the liver and kidney, and the administration of quercetin along with rotenone shown a protective role. This study provides a new insight into where rotenone-induced liver and kidney dysfunction could be successfully protected by quercetin.
Epilepsy is a complex neurological disorder characterized by hypersecretion of excitatory neurotransmitters in the brain. Level ofantioxidant enzymes in the brain changes during seizure. There are many herbal supplements that posses antioxidant potential and might help inprevention and recovery of seizures when used as an adjunct with modern antiepileptic drugs. Objective: The present work was undertaken toevaluate the Ameliorative effect of Sodium valproate in combination with Juglans regia extract against Pentylenetetrazole (PTZ) inducedconvulsions in mice. Materials and Methods: Juglans regia ethanolic extract (JREE) were administered at doses of (200mg/kg and 400 mg/kgp.o) and Sodium Valproate (500mg/kg p.o.) one hour before the administration of PTZ (80mg/kg i.p.). Brain tissues were screened for MDA,Catalase, GSH and protein estimation. Result and Discussion: Administration of JREE in the low and high dose prolongs the onset of myoclonicjerks dose-dependently and also showed protection against PTZ-induced convulsions. PTZ induced seizures caused a significant increase in MDAlevels and a significant decrease in GSH and catalase levels in PTZ group as compared to the vehicle control group. Juglans regia pre-treatmentprevented the oxidative stress as indicated by significant decrease in MDA levels and significant increase in GSH and catalse levels incomparison to PTZ group. Conclusion: The present study showed ameliorative effect of combination of Sodium Valproate in anticonvulsantactivity of ethanolic extract of Juglans regia fruit against PTZ induced seizures and also its protective effect against seizure induced oxidativestress.
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