Study of PMS777, a new type of acetylcholinesterase inhibitor, in human HepG2 cells. Comparison with tacrine and galanthamine on oxidative stress and mitochondrial impairment

Ezoulin, Miezan J.; Dong, Chang‐Zhi; Liu, Z.; Li, J.; Chen, H.Z.; Heymans, Françoise; Lelièvre, L.; Ombetta, Jean-Edouard; Massicot, France

doi:10.1016/j.tiv.2006.01.002

Cited by 26 publications

(40 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Despite the high concentrations used, tacrine itself did not show any effect on the tested cell line (HL60), although other studies have demonstrated that high concentrations of tacrine can induce apoptosis [56] and mitochondrial membrane depolarization [57] in the HepG2 cell line.…”

Section: Biological Studiesmentioning

confidence: 72%

Tacrine derivatives as dual topoisomerase I and II catalytic inhibitors

Janočková

Plsikova

Kovaľ

et al. 2015

Bioorganic Chemistry

View full text Add to dashboard Cite

Section: Biological Studiesmentioning

confidence: 72%

Tacrine derivatives as dual topoisomerase I and II catalytic inhibitors

Janočková

Plsikova

Kovaľ

et al. 2015

Bioorganic Chemistry

View full text Add to dashboard Cite

“…Current neuroprotective treatment options cover all of the molecular targets of the dementia cascades. Interestingly, protective effects of cholinergic agents, especially AChE inhibitors, involve multiple mechanisms (I [48,[127][128][129] ; II [130][131][132] ; III [85,98] ; IV [127,133] ; V [90,133,134] ; references to literature regarding VI and VII can be found throughout this review). Abbreviations: ATP, adenosine triphosphate; CaM, calmodulin; Hup A, huperzine A; JAK/STAT, Janus kinase/signal transducer and activator of transcription; MMP, matrix metalloproteinase; NGF, nerve growth factor; NMDA, N-methyl-D-aspartic acid; PAF, platelet activating factor.…”

Section: Cholinergic Deficiency In Vad Animal Models and Vad Patientsmentioning

confidence: 99%

Cholinergic deficiency involved in vascular dementia: possible mechanism and strategy of treatment

2009

View full text Add to dashboard Cite

Vascular dementia (VaD) is a progressive neurodegenerative disease with a high prevalence. Several studies have recently reported that VaD patients present cholinergic deficits in the brain and cerebrospinal fluid (CSF) that may be closely related to the pathophysiology of cognitive impairment. Moreover, cholinergic therapies have shown promising effects on cognitive improvement in VaD patients. The precise mechanisms of these cholinergic agents are currently not fully understood; however, accumulating evidence indicates that these drugs may act through the cholinergic anti-inflammatory pathway, in which the efferent vagus nerve signals suppress pro-inflammatory cytokine release and inhibit inflammation, although regulation of oxidative stress and energy metabolism, alleviation of apoptosis may also be involved. In this paper, we provide a brief overview of the cholinergic treatment strategy for VaD and its relevant mechanisms of anti-inflammation.

show abstract

“…14.14 , many of the currently commercialized drugs to treat AD are directed against AChE. Several tacrine derivatives, and variants of rivastigmine and xanthostigmine were found to block AChE catalysis of A b aggregation (Bolognesi et al 2004 ;Belluti et al 2005 ;Piazzi et al 2003), and the donepezil derivative, AP2238 (Ezoulin et al 2006 ) . Concerns about hepatotoxicity, due to oxidative damage from metabolism of tacrine (Osseni et al 1999;Dogterom et al 1988 ) , prompted the search for newer compounds that would have the same or better effects on A b aggregation, without toxicity.…”

Section: Acetylcholinesterase Inhibitorsmentioning

confidence: 99%

Strategies for Inhibiting Protein Aggregation: Therapeutic Approaches to Protein-Aggregation Diseases

Lanning

Meredith

2011

Non-Fibrillar Amyloidogenic Protein Assemblies - Common Cytotoxins Underlying Degenerative Diseases

View full text Add to dashboard Cite

Self-aggregation of proteins and peptides is at the root of many diseases, especially neurodegenerative diseases. These conditions include Alzheimer's disease, Huntington's disease, Parkinson's disease, type-2 diabetes mellitus, and transmissible spongiform encephalopathies, which are associated with self-aggregation of amyloid b -protein (A b ), huntingtin, a -synuclein, islet amyloid polypeptide, and the prion protein, respectively. The list of diseases for which protein/peptide aggregation is the root cause is ever expanding. There does not appear to be a single biochemical mechanism by which proteins and peptides self-associate, or a single pathogenic mechanism to explain all protein-/peptide-aggregation diseases. Nevertheless, inhibition of protein self-aggregation remains a potential target for therapeutic intervention. Beyond therapy, inhibitors of protein self-aggregation can serve as tools to help us understand the mechanisms by which aggregation occurs and harms cells. In this chapter, we examine select examples of inhibitors of protein aggregation. We have divided aggregating proteins/peptides into two types: (1) Proteins that have an unstable tertiary structure, that unfold under cellular stress, or that fail to fold correctly during biosynthesis. This instability leads to persistence of unfolded domains that can act as a nidus for self-association. (2) Peptides or proteins (or protein domains) that cannot fold at all, or fold only in the presence of a bound ligand. Examples of the fi rst group include transthyretin, the mammalian prion protein, and certain point-mutant forms of lysozyme or a 1-antitrypsin. In general, self-aggregation of these proteins results from exposure of normally buried hydrophobic residues to aqueous media. Examples of the second group include A b , islet amyloid polypeptide, and calcitonin. Within the second group, we also include proteins that are "peptide-like" in having domains with no unique, stable

show abstract

Study of PMS777, a new type of acetylcholinesterase inhibitor, in human HepG2 cells. Comparison with tacrine and galanthamine on oxidative stress and mitochondrial impairment

Cited by 26 publications

References 34 publications

Tacrine derivatives as dual topoisomerase I and II catalytic inhibitors

Tacrine derivatives as dual topoisomerase I and II catalytic inhibitors

Cholinergic deficiency involved in vascular dementia: possible mechanism and strategy of treatment

Strategies for Inhibiting Protein Aggregation: Therapeutic Approaches to Protein-Aggregation Diseases

Contact Info

Product

Resources

About