Arecoline attenuates memory impairment and demyelination in a cuprizone-induced mouse model of schizophrenia

Xu, Zhizhong; Adilijiang, Abulimiti; Wang, Wenqiang; You, Pan; Lin, Duoduo; Li, Xinmin; He, Jue

doi:10.1097/wnr.0000000000001172

Cited by 20 publications

(13 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Disorders of glucose metabolism in the CNS increase the production of ketone bodies and the activation of additional pathways mediated by free radicals, including NF-kB [7]. According to the literature data, insulin axis impairment and hypometabolism in the CNS cause loss of neurons, astrocytosis, and microgliosis mainly within amygdala and septum [263], axonal damage and demyelination of the hippocampus and fornix [264]. McNay et al indicate that insulin signaling and abnormal glucose transport significantly affect cognitive processes and memory functions regulated by the hippocampus [265].…”

mentioning

confidence: 99%

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

et al. 2020

View full text Add to dashboard Cite

Schizophrenia is a neurodevelopmental disorder featuring chronic, complex neuropsychiatric features. The etiology and pathogenesis of schizophrenia are not fully understood. Oxidative-antioxidant imbalance is a potential determinant of schizophrenia. Oxidative, nitrosative, or sulfuric damage to enzymes of glycolysis and tricarboxylic acid cycle, as well as calcium transport and ATP biosynthesis might cause impaired bioenergetics function in the brain. This could explain the initial symptoms, such as the first psychotic episode and mild cognitive impairment. Another concept of the etiopathogenesis of schizophrenia is associated with impaired glucose metabolism and insulin resistance with the activation of the mTOR mitochondrial pathway, which may contribute to impaired neuronal development. Consequently, cognitive processes requiring ATP are compromised and dysfunctions in synaptic transmission lead to neuronal death, preceding changes in key brain areas. This review summarizes the role and mutual interactions of oxidative damage and impaired glucose metabolism as key factors affecting metabolic complications in schizophrenia. These observations may be a premise for novel potential therapeutic targets that will delay not only the onset of first symptoms but also the progression of schizophrenia and its complications.

show abstract

mentioning

confidence: 99%

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Moreover, in clinical studies, multiple doses of arecoline have been reported to improve the cognitive function of Alzheimer patients [ 79 ]. In a schizophrenic mouse model, arecoline was found to alleviate the memory impairment and demyelination of neurons [ 80 ]. The multiple target approach in herbal medicine primarily focusses on maximizing the therapeutic outcome mediated by multiple compounds on vast array of targets, perhaps promoting the synergism and neutralising toxic effects of each individual compound.…”

Section: Discussionmentioning

confidence: 99%

The Porphyromonas gingivalis inhibitory effects, antioxidant effects and the safety of a Sri Lankan traditional betel quid - an in vitro study

Paranagama

Piyarathne

Nandasena

et al. 2020

BMC Complement Med Ther

View full text Add to dashboard Cite

Background The Sri Lankan traditional betel quid (TBQ) which had been extensively used in the country before its colonization is claimed to have antiperiodontopathic effects in the Sri Lankan folklore. However, there is no reported scientific evidence to support the claimed antiperiodontopathic effects mediated by this TBQ. The present study was carried out to investigate the protective effect of the Sri Lankan TBQ in the pathogenesis of periodontitis. Methods We investigate the ethyl acetate extract of the Sri Lankan TBQ for its antibacterial effects against the keystone periodontopathic bacterium, P. gingivalis and also its antioxidant potential, which is important to protect the periodontium from oxidative stress. Further, its safety was analyzed using the cytokinesis block micronucleus assay on human peripheral blood lymphocytes (PBLs). Results Ethyl acetate extract of this TBQ inhibited the growth of P. gingivalis with a minimum bactericidal concentration (MBC) of 125 μg/ml. It was found to be a rich source of polyphenols and displayed considerable DPPH and ABTS radical scavenging activities and a strong ferric reducing antioxidant power. This extract could protect the cultured human gingival fibroblasts from H 2 O 2 induced oxidative stress. In addition, this TBQ extract was not genotoxic to human PBLs even at a concentration of 2.5 mg/ml. Moreover, it exhibited protective effects against bleomycin induced genotoxicity in PBLs. Conclusion Ethyl acetate extract of the Sri Lankan TBQ is a source of natural antibacterial compounds against P. gingivalis . It is also a source of natural antioxidants which can protect human gingival fibroblasts from H 2 O 2 induced oxidative stress. These properties of the TBQ may have contributed to its claimed antiperiodontopathic effects. Besides, it was found to be relatively non-toxic to human cells. Thus this TBQ extract has a huge potential to be developed as a novel adjunctive therapeutic lead against periodontitis.

show abstract

“…One day after the behavioral test on postnatal day 44, the mice were sacrificed and perfused with 0.1 M PBS (pH 7.4), and the frontal cortex from right hemisphere was dissected, frozen in dry-ice powder and stored at −70°C until used [ 12 ]. The frontal cortex samples from each mouse were homogenized at 4°C in a lysis buffer [50 mM Tris-HCl, 150 mM NaCl, 10 mM EDTA, 10 mM NaF, 1 mM sodium orthovanadate, 1% NP-40, 10 mM sodium pyrophosphate decahydrate, 0.5 mM dithiothreitol, 0.2 mM phenylmethanesulfonyl fluoride, and Complete Mini Protease Inhibitor Cocktail (Roche Diagnostics, Laval, Qc, Canada); pH 7.4].…”

Section: Methodsmentioning

confidence: 99%

Fluoxetine attenuates prepulse inhibition deficit induced by neonatal administration of MK-801 in mice

Yang

Liu²,

Yuan³

et al. 2020

NeuroReport

Self Cite

View full text Add to dashboard Cite

Increasing evidence supports schizophrenia may be a neurodevelopmental and neurodegenerative disorder. Fluoxetine, a selective serotonin reuptake inhibitor, has been reported to have neuroprotective effects and be effective in treating neurodegenerative disorders including schizophrenia. The objective of the present study was to evaluate the effect and underlying neuroprotective mechanism of fluoxetine on the sensorimotor gating deficit, a schizophrenia-like behavior in a neurodevelopmental schizophrenic mouse model induced by MK-801, an N -methyl- d -aspartate glutamate receptor antagonist. On postnatal day 7, mouse pups were treated with a total seven subcutaneous daily injections of MK-801 (1 mg/kg/day), followed by intraperitoneal injection of fluoxetine (5 or 10 mg/kg/day) starting on postnatal day 14 in the MK-801-injected mice for 4 weeks. The sensorimotor gating deficit in mice was measured by prepulse inhibition (PPI) behavioral test on postnatal day 43. After the behavioral test, the protein expression of brain-derived neurotrophic factor (BDNF) was measured by western blot or ELISA in the frontal cortex of mice. Our results showed fluoxetine attenuated PPI deficit and the decrease of cerebral BDNF expression in the MK-801-injected mice. These results suggest that fluoxetine can be used to treat sensorimotor gating deficit in a neurodevelopmental mouse model of schizophrenia, and the attenuating effect of fluoxetine on sensorimotor gating deficit may be related to fluoxetine’s neuroprotective effect targeting on the modulation of cerebral BDNF.

show abstract

Arecoline attenuates memory impairment and demyelination in a cuprizone-induced mouse model of schizophrenia

Cited by 20 publications

References 22 publications

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

The Porphyromonas gingivalis inhibitory effects, antioxidant effects and the safety of a Sri Lankan traditional betel quid - an in vitro study

Fluoxetine attenuates prepulse inhibition deficit induced by neonatal administration of MK-801 in mice

Contact Info

Product

Resources

About