Protective effects of chondroitin sulphate nano-selenium on a mouse model of Alzheimer's disease

Ji, Dongsheng; Xiaming, WU; Li, Delong; Liu, Ping; Zhang, Sitao; Gao, Debo; Gao, Fengmei; Zhang, Mengxiao; Xiao, Yajuan

doi:10.1016/j.ijbiomac.2020.03.079

Cited by 52 publications

(26 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additionally, selenium administration attenuated reduction in DA and its metabolites (DOPAC and HVA) in vivo and in vitro following methamphetamine exposure [53,54]. In agreement with the obtained findings, Ji et al [55] revealed that the neuroprotective impacts of selenium nanoformulations are primarily mediated by the activation of AChE in an Alzheimer's disease model.…”

Section: Discussionsupporting

confidence: 60%

Selenium Nanoparticles with Prodigiosin Rescue Hippocampal Damage Associated with Epileptic Seizures Induced by Pentylenetetrazole in Rats

omairi

Albrakati

Alsharif

et al. 2022

Biology

View full text Add to dashboard Cite

Background: Prodigiosin (PDG) is a red pigment synthesized by bacterial species with important pharmaceutical and biological activities. Here, we investigated the neuroprotective and anticonvulsant activities of green biosynthesized selenium formulations with PDG (SeNPs-PDG) versus pentylenetetrazole (PTZ)-induced epileptic seizures. Methods: Rats were assigned into six experimental groups: control; PTZ (60 mg/kg, epileptic model); sodium valproate (200 mg/kg) + PTZ; PDG (300 mg/kg) + PTZ; sodium selenite (0.5 mg/kg) + PTZ; and SeNPs-PDG (0.5 mg/kg) + PTZ. The treatment duration is extended to 28 days. Results: SeNPs-PDG pre-treatment delayed seizures onset and reduced duration upon PTZ injection. Additionally, SeNPs-PDG enhanced the antioxidant capacity of hippocampal tissue by activating the expression of nuclear factor erythroid 2–related factor 2 and innate antioxidants (glutathione and glutathione derivatives, in addition to superoxide dismutase and catalase) and decreasing the levels of pro-oxidants (lipoperoxidation products and nitric oxide). SeNPs-PDG administration inhibited inflammatory reactions associated with epileptic seizure development by suppressing the production and activity of glial fibrillary acidic protein and pro-inflammatory mediators, including interleukin-1 beta, tumor necrosis factor-alpha, cyclooxygenase-2, inducible nitric oxide synthase, and nuclear factor kappa B. Moreover, SeNPs-PDG protected against hippocampal cell loss following PTZ injection by decreasing the levels of cytosolic cytochrome c, Bax, and caspase-3 and enhancing the expression of anti-apoptotic Bcl-2. Interestingly, SeNPs-PDG restored the PTZ-induced imbalance between excitatory and inhibitory amino acids and improved monoaminergic and cholinergic transmission. Conclusions: These promising antioxidative, anti-inflammatory, anti-apoptotic, and neuromodulatory activities indicate that SeNPs-PDG might serve as a naturally derived anticonvulsant agent.

show abstract

Section: Discussionsupporting

confidence: 60%

Selenium Nanoparticles with Prodigiosin Rescue Hippocampal Damage Associated with Epileptic Seizures Induced by Pentylenetetrazole in Rats

omairi

Albrakati

Alsharif

et al. 2022

Biology

View full text Add to dashboard Cite

show abstract

“…The ability of aluminum to accumulate in sensitive areas of the brain like the hippocampus and frontal cortex made it a possible main contributing factor in the pathogenesis of neurodegenerative disorders [19,20]. Aluminium-mediated neurodegeneration has been well established as an experimental model of AD [21,22], associated with elevated β-amyloid deposition [23], diminished cholinergic transmission, overexpression of phosphorylated Tau [24], and neuronal death [25]. Such a cascade of events in the brain results in cognitive dysfunction resembling AD patients [26].…”

Section: Introductionmentioning

confidence: 99%

Intranasal Oxytocin Attenuates Cognitive Impairment, β-Amyloid Burden and Tau Deposition in Female Rats with Alzheimer’s Disease: Interplay of ERK1/2/GSK3β/Caspase-3

et al. 2022

View full text Add to dashboard Cite

Oxytocin is a neuropeptide hormone that plays an important role in social bonding and behavior. Recent studies indicate that oxytocin could be involved in the regulation of neurological disorders. However, its role in modulating cognition in Alzheimer’s disease (AD) has never been explored. Hence, the present study aims to investigate the potential of chronic intranasal oxytocin in halting memory impairment & AD pathology in aluminum chloride-induced AD in female rats. Morris water maze was used to assess cognitive dysfunction in two-time points throughout the treatment period. In addition, neuroprotective effects of oxytocin were examined by assessing hippocampal acetylcholinesterase activity, β-amyloid 1–42 protein, and Tau levels. In addition, ERK1/2, GSK3β, and caspase-3 levels were assessed as chief neurobiochemical mediators in AD. Hippocampi histopathological changes were also evaluated. These findings were compared to the standard drug galantamine alone and combined with oxytocin. Results showed that oxytocin restored cognitive functions and improved animals’ behavior in the Morris test. This was accompanied by a significant decline in acetylcholinesterase activity, 1–42 β-amyloid and Tau proteins levels. Hippocampal ERK1/2 and GSK3β were also reduced, exceeding galantamine effects, thus attenuating AD pathological hallmarks formation. Determination of caspase-3 revealed low cytoplasmic positivity, indicating the ceasing of neuronal death. Histopathological examination confirmed these findings, showing restored hippocampal cells structure. Combined galantamine and oxytocin treatment showed even better biochemical and histopathological profiles. It can be thus concluded that oxytocin possesses promising neuroprotective potential in AD mediated via restoring cognition and suppressing β-amyloid, Tau accumulation, and neuronal death.

show abstract

“…SOD is a metal enzyme that can catalyze the dismutation of superoxide anions, scavenge O 2 − and repair damaged cells. It is an important enzyme that can scavenge free radicals in the brains of AD mice [64]. SOD levels directly reflect the degree of senescence in mice brain cells [65].…”

Section: Discussionmentioning

confidence: 99%

BDMC protects AD in vitro via AMPK and SIRT1

Xiao

et al. 2020

Translational Neuroscience

View full text Add to dashboard Cite

BackgroundAlzheimer’s disease (AD) is a common neurodegenerative disorder without any satisfactory therapeutic approaches. AD is mainly characterized by the deposition of β-amyloid protein (Aβ) and extensive neuronal cell death. Curcumin, with anti-oxidative stress (OS) and cell apoptosis properties, plays essential roles in AD. However, whether bisdemethoxycurcumin (BDMC), a derivative of curcumin, can exert a neuroprotective effect in AD remains to be elucidated.MethodsIn this study, SK-N-SH cells were used to establish an in vitro model to investigate the effects of BDMC on the Aβ1–42-induced neurotoxicity. SK-N-SH cells were pretreated with BDMC and with or without compound C and EX527 for 30 min after co-incubation with rotenone for 24 h. Subsequently, western blotting, cell viability assay and SOD and GSH activity measurement were performed.ResultsBDMC increased the cell survival, anti-OS ability, AMPK phosphorylation levels and SIRT1 in SK-N-SH cells treated with Aβ1–42. However, after treatment with compound C, an AMPK inhibitor, and EX527, an SIRT1inhibitor, the neuroprotective roles of BDMC on SK-N-SH cells treated with Aβ1–42 were inhibited.ConclusionThese results suggest that BDMC exerts a neuroprotective role on SK-N-SH cells in vitro via AMPK/SIRT1 signaling, laying the foundation for the application of BDMC in the treatment of neurodegenerative diseases related to AMPK/SIRT1 signaling.

show abstract

Protective effects of chondroitin sulphate nano-selenium on a mouse model of Alzheimer's disease

Cited by 52 publications

References 63 publications

Selenium Nanoparticles with Prodigiosin Rescue Hippocampal Damage Associated with Epileptic Seizures Induced by Pentylenetetrazole in Rats

Selenium Nanoparticles with Prodigiosin Rescue Hippocampal Damage Associated with Epileptic Seizures Induced by Pentylenetetrazole in Rats

Intranasal Oxytocin Attenuates Cognitive Impairment, β-Amyloid Burden and Tau Deposition in Female Rats with Alzheimer’s Disease: Interplay of ERK1/2/GSK3β/Caspase-3

BDMC protects AD in vitro via AMPK and SIRT1

Contact Info

Product

Resources

About