Background:Curcumin (Cur), an active ingredient of turmeric is known to have multiple activities, including an antioxidant property and has been suggested to be useful in treatment of several neurological diseases.Objective:To investigate the neuroprotective effects of Cur to mitigate the effect of the Fluoride (F) induced neurotoxicity in mice brain using the histological and the biochemical parameters.Materials and Methods:Exposure of mice (30 days old male) to F (120 ppm) daily for 30 days.Result and Discussion:Treatment with the F causes an increase in lipid peroxidation (LPO) and also increase in the neurodegenerative cells in the hippocampal sub-regions. Interestingly, co-treatment with Cur (30 mg/kg BW) with F (120 ppm) for 30 days results in significant decreases in LPO with a concomitant decrease in neurodegeneration as compared with those treated with F alone.Conclusion:Our study reveals that Cur is useful in ameliorating degenerative effects of F in mice brain.
Nitric oxide (NO) may play a role in the pathophysiology of excitotoxicity. It is also possible that increase in Ca2+ overload and NO-mediated events are involved in neuronal loss during excitotoxicity. Using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry, we have investigated the effects of melatonin on NADPH-d positive hippocampal neurons after kainic acid (KA) induced excitotoxicity in female rats of Wistar strain. Cytosolic Ca2+ (free calcium) in all the respective experimental groups was also studied. Kainic acid was administered, with a single dose of 10 mg/kg/bw (body weight) to the animals. KA treated rats were given melatonin at a dose of 20 mg/kg/bw (for 14 day). On the last day of treatment, animals were transcardially perfused with 4 % paraformaldehyde under deep thiopental anaesthesia. Cryostat sections (20 µm) were cut and stained for NADPH-d positive neurons. KA exposed animals showed a significantly increased number of NADPH-d positive neurons in the dorsal and ventral blade of the dentate gyrus (DG), hilus, CA1 and CA3 area of hippocampus, with a parallel increase in intracellular free Ca2+ ion concentration, as compared to the control group. KA + melatonin-treated animal groups showed reduced number of NADPH-d positive neurons in DG, hilus, CA1 and CA3 areas and a decline in cytosolic Ca2+ concentration, as compared to KA treated group. Our study suggests that the enhanced levels of cytosolic Ca2+ and nitric oxide (NO) play an important role in kainate induced excitotoxicity. Inhibition of NO production may be another means whereby melatonin can reduce oxidative damage and seems to play important role in neuroprotection.
Our study indicates that both antioxidants, curcumin and resveratrol, are useful in reducing neurodegeneration in selective areas of cornus ammonis 1 (CA1), CA3, dentate gyrus (DG) and the cortex of mice brain and in recuperating the loss of memory and learning caused due to fluoride exposure.
Sleep is one of the great unsolved mysteries of biology. It is an important physiological process responsible for the physical, mental and emotional health of a living being. A good sleep is one of the most satisfying human experiences with a role to play in maintaining a good mood and cognitive acuity as well as in promoting physiologic balance and resilience. Chronic sleep deprivation can cause significant and cumulative physiological, neurobehavioral and neurocognitive deficits. Reduced sleep durations are associated with impaired functionality of the brain, thus slowly increase the vulnerability to neuropathology.
Inhibitory effects of a fresh leaf juice of the Withania somnifera (W.s.) on the enzymes acetylcholinesterase (AChE; EC 3.1.17) and nicotinamide adenine dinucleotide diaphorase (NADPH-d) were studied in the mice brain using histochemical and biochemical approaches. The results obtained show significant reduction in the number of and reaction intensity in AChE-and NADPH-d-positive neurons within selected areas of the brains of W.s.-treated mice. Colocalization of AChE and NADPH-d activity also showed significant reduction in the number of cells positive for both enzymes after W.s. treatment, as compared to cells with isolated localization of AChE or NADPH-d. Biochemical estimation of the AChE and NADPH-d levels in brain tissue also showed significant dose-dependent inhibition of the activity of both enzymes after W.s. treatment. In conclusion, our study allows us to suggest that W.s. constituents significantly inhibit both AChE and NADPH-d activity. Inhibition of AChE is direct, while NADPH-d is inhibited indirectly. This study might be important for possible therapeutic use of W.s. in neurodegenerative disorders, in particular in Alzheimer's disease where inhibition of both AChE and nNOS is important.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.