The influence of heterocyclic compound-PAMAM dendrimer complexes on evoked electrical responses in slices of hypoxic brain tissue

Поткин, В. И.; Shcharbin, Dzmitry; Denisov, A. B.; Paschkevich, Svetlana G.; Bryszewska, Maria; Петкевич, С. К.; Клецков, А. В.; Lapotko, Dmitri O.; Казбанов, В. В.; Gurinovich, Tatiana A.; Kulchitsky, Vladimir A.

doi:10.2478/s11658-014-0193-5

Cited by 4 publications

(2 citation statements)

References 12 publications

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“…Previous studies have demonstrated that organic acids and their derivatives can regulate intestinal microflora, and this in turn affects the metabolism and immunity of the organism ( Eyduran et al, 2015 ; Zhang et al, 2018 ). Lipids play an important role in regulating synaptic plasticity, brain metabolism, energy supply, and receptor phenotypes ( Hussain et al, 2020 ), while heterocyclic compounds can improve brain function ( Potkin et al, 2014 ). Therefore, we conducted further analyses to understand the effects of abnormal metabolites on brain function.…”

Section: Discussionmentioning

confidence: 99%

“…Our findings revealed that the purine metabolic pathway was significantly enriched in patients with stroke. Adenosine deaminase is an enzyme involved in purine metabolism and is important for the maintenance of the immune system and for the development and functioning of the central nervous system ( Potkin et al, 2014 ). As normal purine metabolism is particularly important for normal brain function ( Garcia-Esparcia et al, 2015 ), the observation in this study that purine metabolism is significantly enriched in stroke patients is of critical importance in regard to our understanding of the pathogenesis of depression.…”

Section: Discussionmentioning

confidence: 99%

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Intestinal flora induces depression by mediating the dysregulation of cerebral cortex gene expression and regulating the metabolism of stroke patients

Han

Zhao

et al. 2022

Front. Mol. Biosci.

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Post-stroke depression (PSD) is a common cerebrovascular complication characterized by complex pathogenesis and poor treatment effects. Here, we tested the influence of differentially expressed genes (DEGs), non-targeted metabolites, and intestinal microbes on the occurrence and development of PSD. We acquired gene expression profiles for stroke patients, depression patients, and healthy controls from the Gene Expression Omnibus database. After screening for DEGs using differential expression analysis, we identified common DEGs in stroke and depression patients that were considered to form the molecular basis of PSD. Functional enrichment analysis of DEGs also revealed that the majority of biological functions were closely related to metabolism, immunity, the nervous system, and microorganisms, and we also collected blood and stool samples from healthy controls, stroke patients, and PSD patients and performed 16S rDNA sequencing and untargeted metabolomics. After evaluating the quality of the sequencing data, we compared the diversity of the metabolites and intestinal flora within and between groups. Metabolic pathway enrichment analysis was used to identify metabolic pathways that were significantly involved in stroke and PSD, and a global metabolic network was constructed to explore the pathogenesis of PSD. Additionally, we constructed a global regulatory network based on 16S rDNA sequencing, non-targeted metabolomics, and transcriptomics to explore the pathogenesis of PSD through correlation analysis. Our results suggest that intestinal flora associates the dysregulation of cerebral cortex gene expression and could potentially promote the occurrence of depression by affecting the metabolism of stroke patients. Our findings may be helpful in identifying new targets for the prevention and treatment of PSD.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Intestinal flora induces depression by mediating the dysregulation of cerebral cortex gene expression and regulating the metabolism of stroke patients

Han

Zhao

et al. 2022

Front. Mol. Biosci.

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Effect of the isotiazole adjuvants in combination with cisplatin in chemotherapy of neuroepithelial tumors: experimental results and modeling

Potkin,

Pushkarchuk,

Zamaro

et al. 2023

Sci Rep

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Chemotherapy is one of the main treatment options for cancer, but it is usually accompanied with negative side effects. The classical drugs combination with synergistic adjuvants can be the solution to this problem, allowing reducing therapeutic dose. Elucidating the mechanism of adjuvant action is of key importance for the selection of the optimal agent. Here we examine the system drug-adjuvant to explain the observed effect in practice. We used the first line drug cisplatin. Morpholinium and 4-methylpiperazinium 4,5-dichloro isothiazol-3-carboxylates were selected as adjuvants. The study of the cisplatin-adjuvant system was carried out by quantum chemical modeling using DFT. It turned out that adjuvants form conjugates with cisplatin that lead to the relocation of frontier molecular orbitals as well as increase of conjugate’s dipole moment. It resulted in change of the interaction character with DNA and increase of the bioactivity of the system. The data obtained are the basis for expanding the studies to include other drugs and adjuvants. Oncologists will have opportunity to use “classical” chemotherapy drugs in combination with synergists for those patients who have not been previously recommended to such a treatment because of pronounced toxic side effects.

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New derivatives of 4,5-dihydro-1H-pyrazole, 4,5-dihydro-1,2-oxazole, and pyrimidine prepared proceeding from (E)-3-[5-(4-methylphenyl)-1,2-oxazol-3-yl]-1-ferrocenylprop-2-en-1-one

et al. 2017

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Condensation of acetylferrocene with 5-phenyl(4-methylphenyl)-1,2-oxazole-3-carbaldehydes afforded (Е)-3-[5-phenyl(4-methylphenyl)-1,2-oxazol-3-yl]-1-ferrocenylprop-2-en-1-ones. Reactions of (Е)-3-[5-(4-methylphenyl)-1,2-oxazol-3-yl]-1-ferrocenylprop-2-en-1-one with semicarbazide, thiosemicarbazide, and hydroxylamine led to the formation of 5-[5-(4-methylphenyl)-1,2-oxazol-3-yl]-3-ferrocenyl-4,5-dihydro-1Hpyrazole-1-carboxamide, 5-[5-(4-methylphenyl)-1,2-oxazol-3-yl]-3-ferrocenyl-4,5-dihydro-1H-pyrazole-1carbothioamide, and 5-(4-methylphenyl)-3'-ferrocenyl-4',5'-dihydro-3,5'-bi-1,2-oxazole respectively. Reactions of (Е)-3-[5-(4-methylphenyl)-1,2-oxazol-3-yl]-1-ferrocenylprop-2-en-1-one with guanidine and thiourea result in 4-[5-(4-methyl-phenyl)-1,2-oxazol-3-yl]-6-ferrocenylpyrimidin-2-amine and -2-thione respectively.Ferrocene derivatives incorporating in the molecule nitrogen heterocycles, in particular, ferrocenylalkylazoles, exhibit an antitumor activity combined with a low toxicity thus promoting the interest to the synthesis of their new specimens [1-3].We prepared ferrocene derivatives having several N-heterocycles in the a molecule, among them those with 1,2-oxazole. Some functionally substituted isoxazoles alongside with the antitumor action are capable of producing a synergetic effect in compositions with cytostatics used in the tumor chemotherapy thus considerably reducing the dose of the latter and the toxicity for the patient [4][5][6][7][8].The building up of heterocyclic systems is often performed with the use of α,β-unsaturated ketones [9, 10]. Therefore we first obtained 3-[5-phenyl-(4methylphenyl)-1,2-oxazol-3-yl]-1-ferrocenylprop-2-en-1-ones 1 and 2 by condensation of acetylferrocene 3

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The influence of heterocyclic compound-PAMAM dendrimer complexes on evoked electrical responses in slices of hypoxic brain tissue

Cited by 4 publications

References 12 publications

Intestinal flora induces depression by mediating the dysregulation of cerebral cortex gene expression and regulating the metabolism of stroke patients

Intestinal flora induces depression by mediating the dysregulation of cerebral cortex gene expression and regulating the metabolism of stroke patients

Effect of the isotiazole adjuvants in combination with cisplatin in chemotherapy of neuroepithelial tumors: experimental results and modeling

New derivatives of 4,5-dihydro-1H-pyrazole, 4,5-dihydro-1,2-oxazole, and pyrimidine prepared proceeding from (E)-3-[5-(4-methylphenyl)-1,2-oxazol-3-yl]-1-ferrocenylprop-2-en-1-one

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