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Biomolecules
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Novel Synthetic or Natural Neuroprotective Compounds against Oxidative and ER...
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Novel Synthetic or Natural Neuroprotective Compounds against Oxidative and ER Stresses

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Synthetic Biology and Bioengineering".

Deadline for manuscript submissions: closed (4 May 2020) | Viewed by 22444

Special Issue Editor

Prof. Dr. Yoko Hirata

E-Mail Website
Guest Editor
Department of Chemistry and Biomolecular Science, Faculty of Engineering, Gifu University, 1-1 Yanagido, Gifu 501-1193, Japan
Interests: sigma receptors; ER stress; oxidative stress; oxytosis; ferroptosis; dopaminergic neurotoxins; neuroprotective compounds; apoptosis; Parkinson's disease; neurodegeneration
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative and endoplasmic reticulum (ER) stresses are involved in neuronal cell death, eventually leading to neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease. Oxidative and ER stresses are closely associated; reactive oxygen species (ROS), such as the superoxide anion, the hydroxyl radical, and hydrogen peroxide, are generated in multiple organelles, including the ER and mitochondria, as a byproduct of oxidative protein folding and mitochondrial respiration. Although research suggests that some powerful antioxidants can potentially treat Parkinson’s disease and may offer preventive effects, the current medical therapies for neurodegenerative diseases offer symptomatic relief but do not provide a cure or even prevention. Therefore, neuroprotective small molecules that target these stressors and protect neuronal cells from degeneration are critically needed to prevent and treat neurodegenerative diseases.

The molecular mechanisms underlying oxidative- and ER stress-induced cell death are still poorly defined; therefore, studies using various in vitro models of neuronal cell death, including apoptosis, necrosis, ferroptosis/oxytosis, and autophagy, as well as in vivo experimental models, are welcome. In this Special Issue, which is focused on compiling research on “novel synthetic or natural neuroprotective compounds against oxidative and ER stresses” that will be freely accessible online from all over the world, we would like to cover various aspects of our knowledge on small neuroprotective molecules that are effective in preventing neuronal cell death. We are thus welcoming any original research and review articles related to any of these aspects.

We look forward to reading your contributions,

Prof. Yoko Hirata
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • oxidative stress
  • ER stress
  • oxytosis
  • ferroptosis
  • neurodegenerative diseases
  • natural products
  • small molecules

Published Papers (4 papers)

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Research

20 pages, 2880 KiB  
Article
Post-Treatment of Synthetic Polyphenolic 1,3,4 Oxadiazole Compound A3, Attenuated Ischemic Stroke-Induced Neuroinflammation and Neurodegeneration
by Arooj Mohsin Alvi, Lina Tariq Al Kury, Muhammad Umar Ijaz, Fawad Ali Shah, Muhammad Tariq Khan, Ahmed Sadiq Sheikh, Humaira Nadeem, Arif-ullah Khan, Alam Zeb and Shupeng Li
Biomolecules 2020, 10(6), 816; https://doi.org/10.3390/biom10060816 - 26 May 2020
Cited by 45 | Viewed by 5137
Abstract
Ischemic stroke is categorized by either permanent or transient blood flow obstruction, impeding the distribution of oxygen and essential nutrients to the brain. In this study, we examined the neuroprotective effects of compound A3, a synthetic polyphenolic drug product, against ischemic brain injury [...] Read more.
Ischemic stroke is categorized by either permanent or transient blood flow obstruction, impeding the distribution of oxygen and essential nutrients to the brain. In this study, we examined the neuroprotective effects of compound A3, a synthetic polyphenolic drug product, against ischemic brain injury by employing an animal model of permanent middle cerebral artery occlusion (p-MCAO). Ischemic stroke induced significant elevation in the levels of reactive oxygen species and, ultimately, provoked inflammatory cascade. Here, we demonstrated that A3 upregulated the endogenous antioxidant enzymes, such as glutathione s-transferase (GST), glutathione (GSH), and reversed the ischemic-stroke-induced nitric oxide (NO) and lipid peroxidation (LPO) elevation in the peri-infarct cortical and striatal tissue, through the activation of endogenous antioxidant nuclear factor E2-related factor or nuclear factor erythroid 2 (Nrf2). In addition, A3 attenuated neuroinflammatory markers such as ionized calcium-binding adapter molecule-1 (Iba-1), cyclooxygenase-2 (COX-2), tumor necrotic factor-α (TNF-α), toll-like receptors (TLR4), and nuclear factor-κB (NF-κB) by down-regulating p-JNK as evidenced by immunohistochemical results. Moreover, treatment with A3 reduced the infarction area and neurobehavioral deficits. We employed ATRA to antagonize Nrf2, which abrogated the neuroprotective effects of A3 to further assess the possible involvement of the Nrf2 pathway, as demonstrated by increased infarction and hyperexpression of inflammatory markers. Together, our findings suggested that A3 could activate Nrf2, which in turn regulates the downstream antioxidants, eventually mitigating MCAO-induced neuroinflammation and neurodegeneration. Full article
(This article belongs to the Special Issue Novel Synthetic or Natural Neuroprotective Compounds against Oxidative and ER Stresses)
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19 pages, 3085 KiB  
Article
Succinamide Derivatives Ameliorate Neuroinflammation and Oxidative Stress in Scopolamine-Induced Neurodegeneration
by Sumbal Iqbal, Fawad Ali Shah, Komal Naeem, Humaira Nadeem, Sadia Sarwar, Zaman Ashraf, Muhammad Imran, Tariq Khan, Tayyaba Anwar and Shupeng Li
Biomolecules 2020, 10(3), 443; https://doi.org/10.3390/biom10030443 - 13 Mar 2020
Cited by 48 | Viewed by 5580
Abstract
Oxidative stress-mediated neuroinflammatory events are the hallmark of neurodegenerative diseases. The current study aimed to synthesize a series of novel succinamide derivatives and to further investigate the neuroprotective potential of these compounds against scopolamine-induced neuronal injury by in silico, morphological, and biochemical approaches. [...] Read more.
Oxidative stress-mediated neuroinflammatory events are the hallmark of neurodegenerative diseases. The current study aimed to synthesize a series of novel succinamide derivatives and to further investigate the neuroprotective potential of these compounds against scopolamine-induced neuronal injury by in silico, morphological, and biochemical approaches. The characterization of all the succinamide derivatives was carried out spectroscopically via proton NMR (1H-NMR), FTIR and elemental analysis. Further in vivo experiments showed that scopolamine induced neuronal injury, characterized by downregulated glutathione (GSH), glutathione S-transferase (GST), catalase, and upregulated lipid peroxidation (LPO). Moreover, scopolamine increased the expression of inflammatory mediators such as cyclooxygenase2 (COX2), nuclear factor kappa B (NF-kB), tumor necrosis factor (TNF-α), further associated with cognitive impairment. On the other hand, treatment with succinamide derivatives ameliorated the biochemical and immunohistochemical alterations induced by scopolamine, further supported by the results obtained from molecular docking and binding affinities. Full article
(This article belongs to the Special Issue Novel Synthetic or Natural Neuroprotective Compounds against Oxidative and ER Stresses)
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16 pages, 2908 KiB  
Article
Benzimidazole Containing Acetamide Derivatives Attenuate Neuroinflammation and Oxidative Stress in Ethanol-Induced Neurodegeneration
by Muhammad Imran, Lina Tariq Al Kury, Humaira Nadeem, Fawad Ali Shah, Muzaffar Abbas, Shagufta Naz, Arif-ullah Khan and Shupeng Li
Biomolecules 2020, 10(1), 108; https://doi.org/10.3390/biom10010108 - 8 Jan 2020
Cited by 37 | Viewed by 5994
Abstract
Oxidative stress-induced neuroinflammation is the prominent feature of neurodegenerative disorders, and is characterized by a gradual decline of structure and function of neurons. Many biochemical events emerge thanks to the result of this neurodegeneration, and ultimately provoke neuroinflammation, activation of microglia, and oxidative [...] Read more.
Oxidative stress-induced neuroinflammation is the prominent feature of neurodegenerative disorders, and is characterized by a gradual decline of structure and function of neurons. Many biochemical events emerge thanks to the result of this neurodegeneration, and ultimately provoke neuroinflammation, activation of microglia, and oxidative stress, leading to neuronal death. This cascade not only explains the complexity of events taking place across different stages, but also depicts the need for more effective therapeutic agents. The present study was designed to investigate the neuroprotective effects of newly synthesized benzimidazole containing acetamide derivatives, 3a (2-(4-methoxyanilino)-N-[1-(4-methylbenzene-1-sulfonyl)-1H-benzimidazol-2-yl] acetamide) and 3b (2-(Dodecylamino)-N-[1-(4-methylbenzene-1-sulfonyl)-1H-benzimidazol-2-yl] acetamide) against ethanol-induced neurodegeneration in the rat model. Both derivatives were characterized spectroscopically by proton NMR (1H-NMR) and carbon-13 NMR (13C-NMR) and evaluated for neuroprotective potential using different pharmacological approaches. In vivo experiments demonstrated that ethanol triggered neurodegeneration characterized by impaired antioxidant enzymes and elevated oxidative stress. Furthermore, ethanol administration induced neuroinflammation, as demonstrated by elevated expression of tumor necrotic factor (TNF-α), nuclear factor κB (NF-κB), cyclooxygenase-2 (COX2), and ionized calcium-binding adapter molecule-1 (Iba-1), which was further validated by enzyme-linked immunosorbent assay (ELISA). Treatment with 3a and 3b ameliorated the ethanol-induced oxidative stress, neuroinflammation, and memory impairment. The affinity of synthesized derivatives towards various receptors involved in neurodegeneration was assessed through docking analysis. The versatile nature of benzimidazole nucleus and its affinity toward several receptors suggested that it could be a multistep targeting neuroprotectant. As repetitive clinical trials of neuroprotectants targeting a single step of the pathological process have failed previously, our results suggested that a neuroprotective strategy of acting at different stages may be more advantageous to intervene in the vicious cycles of neuroinflammation. Full article
(This article belongs to the Special Issue Novel Synthetic or Natural Neuroprotective Compounds against Oxidative and ER Stresses)
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14 pages, 3332 KiB  
Article
β-Carotene: A Natural Compound Improves Cognitive Impairment and Oxidative Stress in a Mouse Model of Streptozotocin-Induced Alzheimer’s Disease
by Sundas Hira, Uzma Saleem, Fareeha Anwar, Muhammad Farhan Sohail, Zohaib Raza and Bashir Ahmad
Biomolecules 2019, 9(9), 441; https://doi.org/10.3390/biom9090441 - 2 Sep 2019
Cited by 78 | Viewed by 5294
Abstract
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by a cascade of changes in cognitive, behavioral, and social activities. Several areas of the brain are involved in the regulation of memory. Of most importance are the amygdala and hippocampus. Antioxidant therapy is used [...] Read more.
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by a cascade of changes in cognitive, behavioral, and social activities. Several areas of the brain are involved in the regulation of memory. Of most importance are the amygdala and hippocampus. Antioxidant therapy is used for the palliative treatment of different degenerative diseases like diabetes, cirrhosis, and Parkinson’s, etc. The objective of this study was to assess the effectiveness of exogenous antioxidants, in particular, β carotene (1.02 and 2.05 mg/kg) against intracerebroventricular injected streptozotocin-induced memory impairment in mice. Streptozotocin (3 mg/kg, i.c.v) was administered in two separate doses (on 1st and 3rd days of treatment) for neurodegeneration. Fifty Albino mice (male) were selected in the protocol, and they were classified into five groups (Group I—control, Group II—disease, Group III—standard, Group IV–V—β-carotene-treated) to investigate the cognitive enhancement effect of selected antioxidants. The cognitive performance was observed following the elevated plus-maze, passive avoidance, and open field paradigms. Acetylcholine esterase, β-amyloid protein, and biochemical markers of oxidative stress such as glutathione peroxidase, superoxide dismutase, and catalase were analyzed in brain homogenates. In silico activity against acetylcholinesterase (AChE) was determined by the molecular modeling of β-carotene. β-carotene at a dose of 2.05 mg/kg was found to attenuate the deleterious effects of streptozotocin-induced behavioral and biochemical impairments, including the inhibition of acetylcholinesterase activity. The in silico studies confirmed the binding capacity of β-carotene with the acetylcholinesterase enzyme. The administration of β-carotene attenuated streptozotocin-induced cognitive deficit via its anti-oxidative effects, inhibition of acetylcholinesterase, and the reduction of amyloid β-protein fragments. These results suggest that β-carotene could be useful for the treatment of neurodegenerative diseases such as Alzheimer’s disease. Full article
(This article belongs to the Special Issue Novel Synthetic or Natural Neuroprotective Compounds against Oxidative and ER Stresses)
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