Bis(ethylmaltolato)oxidovanadium(<scp>iv</scp>) inhibited the pathogenesis of Alzheimer’s disease in triple transgenic model mice

He, Zhijun; Han, Shuangxue; Wu, Chong; Liu, Lina; Zhu, Hua; Liu, Ang; Lu, Qiping; Huang, Jing-Qiang; Du, Xiubo; Li, Nan; Xie, Qingguo; Wan, Lu; Ni, Jiazuan; Chen, Lingling; Yang, Xinping; Liu, Qiong

doi:10.1039/c9mt00271e

Cited by 23 publications

(14 citation statements)

References 72 publications

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“…BEOV, administered to amyloid mice (TgAPPswe/PS1Δ9) in their drinking water, ameliorated memory and learning deficits, promoted cerebral glucose uptake, protected hippocampal and cortical synapses and reduced Aβ generation and plaque deposition [ 223 ]. Similar findings were observed in the 3xTg model of AD, where BEOV attenuated tau hyperphosphorylation via reducing PTP1B and promoting insulin signalling [ 224 ]. BEOV also attenuated neuroinflammatory processes, and it was shown to inhibit proinflammatory NFκ-B signalling, to inhibit microglial and astrocytic activation and to reduce the cerebral levels of proinflammatory cytokines and inducible nitric oxide synthase (iNOS).…”

Section: Is There Potential In Evaluating Insulin Mimetics For Ad Tre...supporting

confidence: 81%

Current Insights on the Use of Insulin and the Potential Use of Insulin Mimetics in Targeting Insulin Signalling in Alzheimer’s Disease

Woodfield

Gonzales

Helmerhorst

et al. 2022

IJMS

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Alzheimer’s disease (AD) and type 2 diabetes (T2D) are chronic diseases that share several pathological mechanisms, including insulin resistance and impaired insulin signalling. Their shared features have prompted the evaluation of the drugs used to manage diabetes for the treatment of AD. Insulin delivery itself has been utilized, with promising effects, in improving cognition and reducing AD related neuropathology. The most recent clinical trial involving intranasal insulin reported no slowing of cognitive decline; however, several factors may have impacted the trial outcomes. Long-acting and rapid-acting insulin analogues have also been evaluated within the context of AD with a lack of consistent outcomes. This narrative review provided insight into how targeting insulin signalling in the brain has potential as a therapeutic target for AD and provided a detailed update on the efficacy of insulin, its analogues and the outcomes of human clinical trials. We also discussed the current evidence that warrants the further investigation of the use of the mimetics of insulin for AD. These small molecules may provide a modifiable alternative to insulin, aiding in developing drugs that selectively target insulin signalling in the brain with the aim to attenuate cognitive dysfunction and AD pathologies.

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Section: Is There Potential In Evaluating Insulin Mimetics For Ad Tre...supporting

confidence: 81%

Current Insights on the Use of Insulin and the Potential Use of Insulin Mimetics in Targeting Insulin Signalling in Alzheimer’s Disease

Woodfield

Gonzales

Helmerhorst

et al. 2022

IJMS

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show abstract

“…The MWM test was used to check the spatial learning and memory capacities of rats [ 34 ]. Briefly, each rat was trained four times over the course of four days.…”

Section: Methodsmentioning

confidence: 99%

Investigating the Neurotoxic Impacts of Arsenic and the Neuroprotective Effects of Dictyophora Polysaccharide Using SWATH-MS-Based Proteomics

Zhang

Wang

et al. 2022

Molecules

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Arsenic (As) is one of the most important toxic elements in the natural environment. Currently, although the assessment of the potential health risks of chronic arsenic poisoning has received great attention, the research on the effects of arsenic on the brain is still limited. It has been reported that dictyophora polysaccharide (DIP), a common bioactive natural compound found in dietary plants, could reduce arsenic toxicity. Following behavioral research, comparative proteomics was performed to explore the molecular mechanism of arsenic toxicity to the hippocampi of SD (Sprague Dawley) rats and the protective effect of DIP. The results showed that exposure to arsenic impaired the spatial learning and memory ability of SD rats, while DIP treatment improved both the arsenic-exposed rats. Proteomic analysis showed that arsenic exposure dysregulated the expression of energy metabolism, apoptosis, synapse, neuron, and mitochondria related proteins in the hippocampi of arsenic-exposed rats. However, DIP treatment reversed or restored the expression levels of these proteins, thereby improving the spatial learning and memory ability of arsenic-exposed rats. This study is the first to use high-throughput proteomics to reveal the mechanism of arsenic neurotoxicity in rats as well as the protective mechanism of DIP against arsenic neurotoxicity.

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“…Thus, 1 shows promise for intratumoral injections used in treatment of this highly aggressive brain cancer . This finding is particularly important in the light of emerging data on the neuroprotective and neurostimulatory activities of well‐known V IV complexes, including [VO(acac) 2 ] (acac=2,4‐pentanedionato 2− ) and [VO(ema) 2 ] (ema=ethylmaltolato), in contrast with the well‐known neurotoxicity of cisplatin . Decomposition of 1 , [VO(acac) 2 ], or [VO(ema) 2 ] in biological media is likely to lead to similar mixtures of V V ‐ and V IV ‐biomolecule complexes .…”

Section: Methodsmentioning

confidence: 99%

A Short‐Lived but Highly Cytotoxic Vanadium(V) Complex as a Potential Drug Lead for Brain Cancer Treatment by Intratumoral Injections

et al. 2020

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The chemistry and short lifetimes of metal‐based anti‐cancer drugs can be turned into an advantage for direct injections into tumors, which then allow the use of highly cytotoxic drugs. The release of their less toxic decomposition products into the blood will lead to decreased toxicity and can even have beneficial effects. We present a ternary VV complex, 1 ([VOL1L2], where L1 is N‐(salicylideneaminato)‐N′‐(2‐hydroxyethyl)ethane‐1,2‐diamine and L2 is 3,5‐di‐tert‐butylcatechol), which enters cells intact to induce high cytotoxicity in a range of human cancer cells, including T98g (glioma multiforme), while its decomposition products in cell culture medium were ≈8‐fold less toxic. 1 was 12‐fold more toxic than cisplatin in T98g cells and 6‐fold more toxic in T98g cells than in a non‐cancer human cell line, HFF‐1. Its high toxicity in T98g cells was retained in the presence of physiological concentrations of the two main metal‐binding serum proteins, albumin and transferrin. These properties favor further development of 1 for brain cancer treatment by intratumoral injections.

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Bis(ethylmaltolato)oxidovanadium(iv) inhibited the pathogenesis of Alzheimer’s disease in triple transgenic model mice

Abstract: BEOV activates PPARγ to affect JAK2/STAT3/SOCS1 signaling and eventually prevents Aβ generation. Meanwhile, BEOV inactivates PTP1B to affect PI3K/Akt/GSK3β signaling and finally reduces tau hyperphosphorylation.

Cited by 23 publications

References 72 publications

Current Insights on the Use of Insulin and the Potential Use of Insulin Mimetics in Targeting Insulin Signalling in Alzheimer’s Disease

Current Insights on the Use of Insulin and the Potential Use of Insulin Mimetics in Targeting Insulin Signalling in Alzheimer’s Disease

Investigating the Neurotoxic Impacts of Arsenic and the Neuroprotective Effects of Dictyophora Polysaccharide Using SWATH-MS-Based Proteomics

A Short‐Lived but Highly Cytotoxic Vanadium(V) Complex as a Potential Drug Lead for Brain Cancer Treatment by Intratumoral Injections

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