Curcumin Exerts Neuroprotective Effects Against Homocysteine Intracerebroventricular Injection-Induced Cognitive Impairment and Oxidative Stress in Rat Brain

Objective: Oxidative stress appears to be an early event involved in the pathogenesis of Alzheimer's disease (AD). The present study was designed to investigate the neuroprotective effects of citrullus lanatus on bilateral common carotid artery occlusion (BCCAO) induced cognitive impairment and oxidative stress in Wistar albino rats. Methods: Cognitive impairment and oxidative stress were induced by BCCAO for 30 min, followed by 7 d reperfusion of male wistar rats. Morris water maze and rectangular maze performance tests and locomotor activity were used to assess memory performance tasks. To study the activity, rats weighing 250-300g were pre-treated with successive extracts of n-hexane fraction (HF), ethyl acetate fraction (EAF), ethanol fraction (EF) and aqueous fraction (AF) of 400 mg/kg, 200 mg/kg, p. o of each for 10 d and the treatment was continued for another 7 d after cerebral ischemia. Various biochemical parameters like lipid peroxidation, Catalase, DPPH and AchE were also estimated in the brain after the treatment. Results: There was significantly increased oxidative stress and cholinesterase activity with cognitive decline in the hippocampus in rats of BCCAO group as compared to sham-operated (p<0.05). The animals treated with Donepezil, HF and EF prevented the biochemical changes significantly (p<0.001) and there was significant (p<0.001) improvement in cognitive parameters compared to BCCAO treated rats. Conclusion: Thus present study indicates the neuroprotective effect of citrulus lanatus seed extract (HF and EF) against BCCAO induced cognitive impairment and associative oxidative damage.

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NXP032 Ameliorates Aging-Induced Oxidative Stress and Cognitive Impairment in Mice through Activation of Nrf2 Signaling

Antioxidants ◽

10.3390/antiox11010130 ◽

2022 ◽

Vol 11 (1) ◽

pp. 130

Author(s):

Jae-Min Lee ◽

Joo Hee Lee ◽

Min Kyung Song ◽

Youn-Jung Kim

Keyword(s):

Oxidative Stress ◽

Cognitive Impairment ◽

Vitamin C ◽

Neuronal Damage ◽

Chemical Properties ◽

Brain Regions ◽

Dna Aptamer ◽

Antioxidant Vitamin ◽

Neuroprotective Effects ◽

And Oxidative Stress

Aging is a neurodegenerative disease that leads to cognitive impairment, and an increase in oxidative stress as a major cause is an important factor. It has been reported that aging-related cognitive impairment is associated with increased oxidative damage in several brain regions during aging. As a powerful antioxidant, vitamin C plays an important role in preventing oxidative stress, but due to its unstable chemical properties, it is easily oxidized and thus the activity of antioxidants is reduced. In order to overcome this easily oxidized vulnerability, we developed NXP032 (vitamin C/DNA aptamer complex) that can enhance the antioxidant efficacy of vitamin C using an aptamer. We developed NXP032 (vitamin C/DNA Aptamin C320 complex) that can enhance the antioxidant efficacy of vitamin C using an aptamer. In the present study, we evaluated the neuroprotective effects of NXP032 on aging-induced cognitive decline, oxidative stress, and neuronal damage in 17-month-old female mice. NXP032 was orally administered at 200 mg/kg of ascorbic acid and 4 mg/kg of DNA aptamer daily for eight weeks. Before the sacrifice, a cognitive behavioral test was performed. Administration of NXP032 alleviated cognitive impairment, neuronal damage, microglia activity, and oxidative stress due to aging. We found that although aging decreases the Nrf2-ARE pathway, NXP032 administration activates the Nrf2-ARE pathway to increase the expression of SOD-1 and GSTO1/2. The results suggest that the new aptamer complex NXP032 may be a therapeutic intervention to alleviate aging-induced cognitive impairment and oxidative stress.

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Centella asiatica Alleviates AlCl3-induced Cognitive Impairment, Oxidative Stress, and Neurodegeneration by Modulating Cholinergic Activity and Oxidative Burden in Rat Brain

Biological Trace Element Research ◽

10.1007/s12011-021-03083-5 ◽

2022 ◽

Author(s):

Zeba Firdaus ◽

Devendra Kumar ◽

Sushil Kumar Singh ◽

Tryambak Deo Singh

Keyword(s):

Oxidative Stress ◽

Cognitive Impairment ◽

Rat Brain ◽

Centella Asiatica ◽

Cholinergic Activity

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Harpagophytum Procumbens Ethyl Acetate Fraction Reduces Fluphenazine-Induced Vacuous Chewing Movements and Oxidative Stress in Rat Brain

Neurochemical Research ◽

10.1007/s11064-015-1811-y ◽

2016 ◽

Vol 41 (5) ◽

pp. 1170-1184 ◽

Cited By ~ 2

Author(s):

Larissa Finger Schaffer ◽

Catiuscia Molz de Freitas ◽

Ana Paula Chiapinotto Ceretta ◽

Luis Ricardo Peroza ◽

Elizete de Moraes Reis ◽

...

Keyword(s):

Oxidative Stress ◽

Ethyl Acetate ◽

Rat Brain ◽

Ethyl Acetate Fraction ◽

Vacuous Chewing Movements ◽

Harpagophytum Procumbens ◽

Vacuous Chewing ◽

And Oxidative Stress

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Rapamycin attenuated zinc-induced tau phosphorylation and oxidative stress in animal model: Involvement of dual mTOR/p70S6K and Nrf2/HO-1 pathways

10.1101/2021.09.24.461637 ◽

2021 ◽

Author(s):

Chencen Lai ◽

Qian Chen ◽

Yuanting Ding ◽

Songbai Su ◽

Heng Liu ◽

...

Keyword(s):

Oxidative Stress ◽

Cognitive Impairment ◽

Morris Water Maze ◽

Zinc Sulfate ◽

Water Maze ◽

Tau Phosphorylation ◽

Alzheimers Disease ◽

Tau Pathology ◽

Biochemical Assays ◽

And Oxidative Stress

Alzheimers disease is pathologically featured by abnormal accumulation of amyloid-beta plaque, neurofibrillary tangles, oxidative stress, neuroinflammation, and neurodegeneration. Metal dysregulation including excessive zinc released by presynaptic neurons plays an important role in tau pathology and oxidase activation. The activities of mammalian target of rapamycin (mTOR)/ ribosomal S6 protein kinase (p70S6K) are elevated in the brains of patients with Alzheimers disease. Zinc induces tau hyperphosphorylation via mTOR/P70S6K activation in vitro. However, the involvement of mTOR/P70S6K pathway in zinc-induced oxidative stress, tau degeneration, synaptic and cognitive impairment, has not been fully elucidated in vivo. Here we assessed in the effect of pathological concentration of zinc in SH-SY5Y cells by using biochemical assays and immunofluorescence staining. Rats (n = 18, male) were lateral ventricularly-injected with zinc and treated with rapamycin (intraperitoneal injection) for one week and assessed using Morris water maze. Evaluation of the oxidative stress, tau phorsphylation and synaptic impairment were performed using the hippocampus tissue of the rats by biochemical assays and immunofluorescence staining. Results from Morris water maze showed that the capacity of spatial memory is impaired in zinc-treated rats. Zinc sulfate significantly increased the levels of P-mTOR Ser2448, P-p70S6K Thr389, and P-tau Ser356, and decreased levels of Nrf2 and HO-1 in SH-SY5Y cells and in zinc-treated rats compared with control groups. Increased expressions of reactive oxygen species were observed in zinc sulfate-induced SH-SY5Y cells as well as in the hippocampus of zinc-injected rats. Rapamycin, an inhibitor of mTOR, rescued the zinc-induced increases in mTOR/p70S6K activations, tau phosphorylation and oxidative stress, as well as Nrf2/HO-1 inactivation, cognitive impairment and synaptic impairment reduced the expression of synapse-related proteins in zinc-injected rats. In conclusion, our findings imply that rapamycin prevents zinc-induced cognitive impairment and protects neurons from tau pathology, oxidative stress and synaptic impairment, by decreasing mTOR/p70S6K hyperactivity and increasing Nrf2/HO-1 activity.

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