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Therapeutic Potentials of Natural Products on Cerebrovascular Diseases and Neurodegeneration
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Therapeutic Potentials of Natural Products on Cerebrovascular Diseases and Neurodegeneration

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 8326

Special Issue Editor

Prof. Dr. Yuh-Fung Chen

E-Mail Website
Guest Editor
Deputy Director of Library and Information Center, Dept Pharmacology, China Medical University, Taichung City, Taiwan
Interests: in vitro models of neuroinflammation; in vivo rodent models of ischemic stroke; translational neuroscience research of natural products (botanicals and medicinal herbs)

Special Issue Information

Dear Colleagues, 

Cerebrovascular stroke is the leading cause of death and disability globally. After a stroke survives, it usually leaves different degrees of neurological dysfunction, and some are even related to brain degeneration (dementia). According to the World Health Organization, the percentage of brain degeneration over the age of 60 in the world is 5–8%. Dementia is one neurodegeneration group; Huntington's disease and Parkinson's disease are included in neurodegeneration. Neurodegeneration is characterized by progressive dysfunction and loss of neuronal structure and is associated with numerous pathological processes. Brain inflammation and loss of neurons also underline the pathology. Oxidative stress as one of the pathogenesis of cerebrovascular diseases and neurodegeneration has been implicated. Strategies for preventing and ameliorating cerebrovascular and neurodegeneration include preventing cell death and restoring the function of damaged neurons. Natural products have neuroprotective effects via multiple action mechanisms, and the use of natural products may provide great potential opportunities.

This special issue on “Therapeutic Potentials of Natural Products on Cerebrovascular Diseases and Neurodegeneration” will cover original research manuscripts, updated reviews, or communications on topics related to the potential roles of natural products against the pathophysiology of cerebrovascular diseases and neurodegeneration. In addition, papers focused on the impact of natural products on neurodegeneration or cerebrovascular diseases are welcome for this Special Issue.

Prof. Dr. Yuh-Fung Chen
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • cerebrovascular diseases
  • stroke
  • neurodegeneration
  • dementia
  • Huntington’s disease
  • Parkinson’s disease
  • natural products
  • neuroprotection

Published Papers (3 papers)

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Research

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13 pages, 3401 KiB  
Article
Trilinolein, a Natural Triacylglycerol, Protects Cerebral Ischemia through Inhibition of Neuronal Apoptosis and Ameliorates Intimal Hyperplasia via Attenuation of Migration and Modulation of Matrix Metalloproteinase-2 and RAS/MEK/ERK Signaling Pathway in VSMCs
by Yuh-Fung Chen, Kuo-Jen Wu, Lian-Ru Siao and Huei-Yann Tsai
Int. J. Mol. Sci. 2022, 23(21), 12820; https://doi.org/10.3390/ijms232112820 - 24 Oct 2022
Cited by 8 | Viewed by 1854
Abstract
Cerebrovascular disease is one of the leading causes of disability and death worldwide, and seeking a potential treatment is essential. Trilinolein (TriL) is a natural triacylglycerol presented in several plants. The effects of TriL on cerebrovascular diseases such as cerebral ischemia and carotid [...] Read more.
Cerebrovascular disease is one of the leading causes of disability and death worldwide, and seeking a potential treatment is essential. Trilinolein (TriL) is a natural triacylglycerol presented in several plants. The effects of TriL on cerebrovascular diseases such as cerebral ischemia and carotid stenosis have never been studied. Accordingly, we investigated the protection of TriL on cerebral ischemia/reperfusion (I/R) and vascular smooth muscle cell (VSMC) migration in vivo and in vitro. The cerebral infarction area, the intima to media area (I/M ratio), and proliferating cell nuclear antigen (PCNA)-staining of the carotid artery were measured. Platelet-derived growth factor (PDGF)-BB-stimulated A7r5 cell migration and potential mechanisms of TriL were investigated by wound healing, transwell, and Western blotting. TriL (50, 100, and 200 mg/kg, p.o.) reduced: the cerebral infarction area; neurological deficit; TUNEL-positive apoptosis; intimal hyperplasia; and PCNA-positive cells in rodents. TriL (5, 10, and 20 µM) significantly inhibited PDGF-BB-stimulated A7r5 cell migration and reduced matrix metalloproteinase-2 (MMP-2), Ras, MEK, and p-ERK protein levels in PDGF-BB-stimulated A7r5 cells. TriL is protective in models of I/R-induced brain injury, carotid artery ligation-induced intimal hyperplasia, and VSMC migration both in vivo and in vitro. TriL could be potentially efficacious in preventing cerebral ischemia and cerebrovascular diseases. Full article
(This article belongs to the Special Issue Therapeutic Potentials of Natural Products on Cerebrovascular Diseases and Neurodegeneration)
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Review

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27 pages, 3617 KiB  
Review
Medicinal Herbs and Their Derived Ingredients Protect against Cognitive Decline in In Vivo Models of Alzheimer’s Disease
by Yueh-Ting Tsai, Shung-Te Kao and Chin-Yi Cheng
Int. J. Mol. Sci. 2022, 23(19), 11311; https://doi.org/10.3390/ijms231911311 - 25 Sep 2022
Cited by 6 | Viewed by 3102
Abstract
Alzheimer’s disease (AD) has pathological hallmarks including amyloid beta (Aβ) plaque formation. Currently approved single-target drugs cannot effectively ameliorate AD. Medicinal herbs and their derived ingredients (MHDIs) have multitarget and multichannel properties, engendering exceptional AD treatment outcomes. This review delineates how in in [...] Read more.
Alzheimer’s disease (AD) has pathological hallmarks including amyloid beta (Aβ) plaque formation. Currently approved single-target drugs cannot effectively ameliorate AD. Medicinal herbs and their derived ingredients (MHDIs) have multitarget and multichannel properties, engendering exceptional AD treatment outcomes. This review delineates how in in vivo models MHDIs suppress Aβ deposition by downregulating β- and γ-secretase activities; inhibit oxidative stress by enhancing the antioxidant activities and reducing lipid peroxidation; prevent tau hyperphosphorylation by upregulating protein phosphatase 2A expression and downregulating glycogen synthase kinase-3β expression; reduce inflammatory mediators partly by upregulating brain-derived neurotrophic factor/extracellular signal-regulated protein kinase 1/2-mediated signaling and downregulating p38 mitogen-activated protein kinase (p38 MAPK)/c-Jun N-terminal kinase (JNK)-mediated signaling; attenuate synaptic dysfunction by increasing presynaptic protein, postsynaptic protein, and acetylcholine levels and preventing acetylcholinesterase activity; and protect against neuronal apoptosis mainly by upregulating Akt/cyclic AMP response element-binding protein/B-cell lymphoma 2 (Bcl-2)-mediated anti-apoptotic signaling and downregulating p38 MAPK/JNK/Bcl-2-associated x protein (Bax)/caspase-3-, Bax/apoptosis-inducing factor-, C/EBP homologous protein/glucose-regulated protein 78-, and autophagy-mediated apoptotic signaling. Therefore, MHDIs listed in this review protect against Aβ-induced cognitive decline by inhibiting Aβ accumulation, oxidative stress, tau hyperphosphorylation, inflammation, synaptic damage, and neuronal apoptosis in the cortex and hippocampus during the early and late AD phases. Full article
(This article belongs to the Special Issue Therapeutic Potentials of Natural Products on Cerebrovascular Diseases and Neurodegeneration)
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29 pages, 4362 KiB  
Review
Therapeutic Potential and Mechanisms of Novel Simple O-Substituted Isoflavones against Cerebral Ischemia Reperfusion
by Shu-Er Yang, Jin-Cherng Lien, Chia-Wen Tsai and Chi-Rei Wu
Int. J. Mol. Sci. 2022, 23(18), 10394; https://doi.org/10.3390/ijms231810394 - 8 Sep 2022
Cited by 6 | Viewed by 2863
Abstract
Isoflavones have been widely studied and have attracted extensive attention in fields ranging from chemotaxonomy and plant physiology to human nutrition and medicine. Isoflavones are often divided into three subgroups: simple O-substituted derivatives, prenylated derivatives, and glycosides. Simple O-substituted isoflavones and their glycosides, [...] Read more.
Isoflavones have been widely studied and have attracted extensive attention in fields ranging from chemotaxonomy and plant physiology to human nutrition and medicine. Isoflavones are often divided into three subgroups: simple O-substituted derivatives, prenylated derivatives, and glycosides. Simple O-substituted isoflavones and their glycosides, such as daidzein (daidzin), genistein (genistin), glycitein (glycitin), biochanin A (astroside), and formononetin (ononin), are the most common ingredients in legumes and are considered as phytoestrogens for daily dietary hormone replacement therapy due to their structural similarity to 17-β-estradiol. On the basis of the known estrogen-like potency, these above isoflavones possess multiple pharmacological activities such as antioxidant, anti-inflammatory, anticancer, anti-angiogenetic, hepatoprotective, antidiabetic, antilipidemic, anti-osteoporotic, and neuroprotective activities. However, there are very few review studies on the protective effects of these novel isoflavones and their related compounds in cerebral ischemia reperfusion. This review primarily focuses on the biosynthesis, metabolism, and neuroprotective mechanism of these aforementioned novel isoflavones in cerebral ischemia reperfusion. From these published works in in vitro and in vivo studies, simple O-substituted isoflavones could serve as promising therapeutic compounds for the prevention and treatment of cerebral ischemia reperfusion via their estrogenic receptor properties and neuron-modulatory, antioxidant, anti-inflammatory, and anti-apoptotic effects. The detailed mechanism of the protective effects of simple O-substituted isoflavones against cerebral ischemia reperfusion might be related to the PI3K/AKT/ERK/mTOR or GSK-3β pathway, eNOS/Keap1/Nrf-2/HO-1 pathway, TLRs/TIRAP/MyD88/NFκ-B pathway, and Bcl-2-regulated anti-apoptotic pathway. However, clinical trials are needed to verify their potential on cerebral ischemia reperfusion because past studies were conducted with rodents and prophylactic administration. Full article
(This article belongs to the Special Issue Therapeutic Potentials of Natural Products on Cerebrovascular Diseases and Neurodegeneration)
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