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Bioactive Compounds in Human Brain Structures and Diseases: 2nd Edition
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Bioactive Compounds in Human Brain Structures and Diseases: 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 20 September 2025 | Viewed by 3892

Special Issue Editor

Dr. Terezia Kiskova

E-Mail Website
Guest Editor
Institute of Pathology, Faculty of Medicine, Pavol Jozef Safarik University, 040 01 Kosice, Slovakia
Interests: brain cancer; molecular mechanism; natural compounds
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Brain diseases are the leading cause of DALYs and the second-leading cause of death. As the brain is a vulnerable structure, it may be damaged during development as well as during adulthood. This Special Issue is focused on exploring how various bioactive compounds may lead to neuroprotection of the brain and prevent/treat brain diseases, such as neurodegenerative disorders, ischemic attacks, brain cancer, or depression.

This Special Issue welcomes original research and review papers demonstrating the molecular mechanisms of neuroprotection against brain injury using in vivo or in vitro models of animals, as well as studies conducted in clinical settings.

Dr. Terézia Kisková
Guest Editor

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Keywords

  • brain
  • brain cancer
  • depression
  • neurodegenerative disorders
  • natural compounds

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Published Papers (3 papers)

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Research

18 pages, 4486 KiB  
Article
Ibuprofen Does Not Prevent Inhibition of Fetal Breathing Movements Caused by Intrauterine Inflammation in Fetal Sheep
by Nhi T. Tran, Vanesa Stojanovska, Sharmony B. Kelly, Kayla Vidinopoulos, John Atta, Eva Matthews-Staindl, Valerie A. Zahra, Yen Pham, Eric A. P. Herlenius, Stuart B. Hooper, Beth J. Allison, Robert Galinsky and Graeme R. Polglase
Int. J. Mol. Sci. 2025, 26(12), 5591; https://doi.org/10.3390/ijms26125591 - 11 Jun 2025
Viewed by 216
Abstract
Antenatal inflammation/infection is a major cause of neonatal apnoea and hypoventilation. Prostaglandin E2 (PGE2) is a key inflammatory mediator associated with depression of fetal and neonatal breathing. We aimed to determine whether antenatal ibuprofen, a cyclooxygenase inhibitor that reduces synthesis of [...] Read more.
Antenatal inflammation/infection is a major cause of neonatal apnoea and hypoventilation. Prostaglandin E2 (PGE2) is a key inflammatory mediator associated with depression of fetal and neonatal breathing. We aimed to determine whether antenatal ibuprofen, a cyclooxygenase inhibitor that reduces synthesis of PGE2, restores fetal breathing movements (FBM) in late-gestation fetal sheep exposed to systemic lipopolysaccharide (LPS). Fetal sheep (125 days gestation, d; term ~148 d) were instrumentally monitored for continuous measurement of FBM and physiological parameters. At 130 d fetuses were randomly allocated between groups receiving i.v. saline (CTLSAL, n = 9), escalating doses of LPS (i.v.) over 3 days (LPSSAL, n = 8), or ibuprofen one hour after each LPS dose (LPSIBU, n = 8). Regular plasma samples were collected for PGE2 assessment. At 135 d, cerebrospinal fluid and brainstem tissue were collected at autopsy for assessments of PGE2 expression, and immunohistochemical quantification of astrocytes and microglia within key brainstem respiratory centres was performed to assess inflammation. LPS exposure increased PGE2 levels in plasma, cerebrospinal fluid and the RTN/pFRG (p < 0.05) and decreased the incidence, amplitude and amount of the accentuated (>5 mmHg) FBMs. Ibuprofen reduced plasma and RTN/pFRG PGE2 expression (p < 0.01 and p = 0.031, respectively) but did not restore FBMs. Astrocyte and microglial density increased in the RTN/pFRG, NTS and raphe nucleus in LPSIBU fetuses, compared to LPSSAL (p < 0.05). Antenatal ibuprofen treatment did not restore depressed FBM, despite reducing the circulating and brainstem PGE2 levels in LPS-exposed fetal sheep. Other inflammatory pathways or more specific targeting of PGE2 may be more effective in preventing apnoea caused by exposure to intrauterine infection/inflammation. Full article
(This article belongs to the Special Issue Bioactive Compounds in Human Brain Structures and Diseases: 2nd Edition)
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17 pages, 4727 KiB  
Article
The Antidepressant Effect of Resveratrol Is Related to Neuroplasticity Mediated by the ELAVL4-Bdnf mRNA Pathway
by Hailong Ge, Lujia Si, Chen Li, Junjie Huang, Limin Sun, Lan Wu, Yinping Xie, Ling Xiao and Gaohua Wang
Int. J. Mol. Sci. 2025, 26(3), 1113; https://doi.org/10.3390/ijms26031113 - 27 Jan 2025
Viewed by 1581
Abstract
Resveratrol, a plant-derived polyphenol, exhibits significant antidepressant effects and notably enhances neuroplasticity in neurological diseases. However, whether the antidepressant function of resveratrol is related to neuroplasticity remains uncertain, and the underlying mechanisms is poorly understood. This study aims to investigate the role and [...] Read more.
Resveratrol, a plant-derived polyphenol, exhibits significant antidepressant effects and notably enhances neuroplasticity in neurological diseases. However, whether the antidepressant function of resveratrol is related to neuroplasticity remains uncertain, and the underlying mechanisms is poorly understood. This study aims to investigate the role and mechanism of resveratrol in neuroplasticity in depression. Here, we adopted the chronic unpredictable mild stress (CUMS) model and resveratrol intervention by oral gavage. Thereafter, behavioral tests confirmed resveratrol’s antidepressant effect, and Nissl staining, Golgi staining, and Western blotting (WB) were employed to assess the neuronal plasticity. Moreover, proteomic analysis and WB were used to screen and identify the key proteins. To investigate the downstream target of ELAV-like RNA-binding protein 4 (ELAVL4) (one of candidate genes), the RNA Interactome Database and the National Center for Biotechnology Information databases were utilized to predict the targets of ELAVL4. Finally, Quantitative PCR, WB, and Immunofluorescence were used to verify the prediction. Our results indicate that resveratrol alleviates CUMS-induced depressive-like behaviors accompanied by the restoration of impaired hippocampal neuroplasticity. Then, proteomic analysis shows that 351 differentially expressed proteins (DEPs) decrease after CUMS, while 24 DEPs increase remarkably with the resveratrol treatment. Among which, ELAVL4 is downregulated by CUMS, simultaneously increasing after resveratrol intervention, which acts as a protective protein in this process. Finally, brain-derived neurotrophic factor (Bdnf) mRNA is predicted to be the potential target of ELAVL4 and validated by molecular technologies. In conclusion, our findings demonstrate that resveratrol’s antidepressant efficacy is closely associated with ELAVL4, an RNA-binding protein, a mediated neuroplasticity pathway, potentially intersecting with the Bdnf mRNA. Overall, this research sheds light on the role of the ELAVL4-Bdnf mRNA pathway through neuroplasticity in resveratrol’s antidepressant action, which provides an mRNA regulation perspective for the development of novel antidepressants and understanding depression pathology. Full article
(This article belongs to the Special Issue Bioactive Compounds in Human Brain Structures and Diseases: 2nd Edition)
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21 pages, 3175 KiB  
Article
The First In Vivo Study Shows That Gyrophoric Acid Changes Behavior of Healthy Laboratory Rats
by Patrik Simko, Andrea Leskanicova, Maria Suvakova-Nunhart, Jan Koval, Nela Zidekova, Martina Karasova, Petra Majerova, Ludmila Verboova, Alzbeta Blicharova, Martin Kertys, Ivan Barvik, Andrej Kovac and Terezia Kiskova
Int. J. Mol. Sci. 2024, 25(12), 6782; https://doi.org/10.3390/ijms25126782 - 20 Jun 2024
Cited by 1 | Viewed by 1386
Abstract
Gyrophoric acid (GA), a lichen secondary metabolite, has attracted more attention during the last years because of its potential biological effects. Until now, its effect in vivo has not yet been demonstrated. The aim of our study was to evaluate the basic physicochemical [...] Read more.
Gyrophoric acid (GA), a lichen secondary metabolite, has attracted more attention during the last years because of its potential biological effects. Until now, its effect in vivo has not yet been demonstrated. The aim of our study was to evaluate the basic physicochemical and pharmacokinetic properties of GA, which are directly associated with its biological activities. The stability of the GA in various pH was assessed by conducting repeated UV-VIS spectral measurements. Microsomal stability in rat liver microsomes was performed using Ultra-Performance LC/MS. Binding to human serum albumin (HSA) was assessed using synchronous fluorescence spectra, and molecular docking analysis was used to reveal the binding site of GA to HSA. In the in vivo experiment, 24 Sprague-Dawley rats (Velaz, Únetice, Czech Republic) were used. The animals were divided as follows. The first group (n = 6) included healthy males as control intact rats (♂INT), and the second group (n = 6) included healthy females as controls (♀INT). Groups three and four (♂GA/n = 6 and ♀GA/n = 6) consisted of animals with daily administered GA (10 mg/kg body weight) in an ethanol-water solution per os for a one-month period. We found that GA remained stable under various pH and temperature conditions. It bonded to human serum albumin with the binding constant 1.788 × 106 dm3mol−1 to reach the target tissue via this mechanism. In vivo, GA did not influence body mass gain, food, or fluid intake during the experiment. No liver toxicity was observed. However, GA increased the rearing frequency in behavioral tests (p < 0.01) and center crossings in the elevated plus-maze (p < 0.01 and p < 0.001, respectively). In addition, the time spent in the open arm was prolonged (p < 0.01 and p < 0.001, respectively). Notably, GA was able to pass through the blood–brain barrier, indicating its ability to permeate into the brain and to stimulate neurogenesis in the hilus and subgranular zone of the hippocampus. These observations highlight the potential role of GA in influencing brain function and neurogenesis. Full article
(This article belongs to the Special Issue Bioactive Compounds in Human Brain Structures and Diseases: 2nd Edition)
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