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Pharmaceuticals
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Natural Products for Potential Use of Neuroprotective and Neurorestorative Effects...
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Natural Products for Potential Use of Neuroprotective and Neurorestorative Effects in Stroke

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Natural Products".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 12663

Special Issue Editors

Dr. Hansen Chen

E-Mail Website1 Website2
Guest Editor
Department of Neurosurgery, School of Medicine, Stanford University, Stanford, CA, USA
Interests: stroke; blood–brain barrier; neuroinflammation; oxidative stress; natural compounds; stem cell
Special Issues, Collections and Topics in MDPI journals
Dr. Qingkun Liu

E-Mail Website
Guest Editor
Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA
Interests: microglia; systemic immune responses; neurogenesis; neurodegeneration; peripheral immune suppression; etc.

Special Issue Information

Dear Colleagues,

We are launching a Special Issue that focuses on the most recent advances in natural product research for treating ischemic stroke, from acute ischemic stroke protection to post-stroke recovery. Stroke remains one of the leading causes of mortality and morbidity around the world, yet treatment options are very limited. Recent research revealed the potential of natural products to minimize stroke injury and promote stroke recovery. In this Special Issue, we aim to provide the most recent updates on natural product research for treating stroke involving both the nervous system and immune system, which will include in vitro, in vivo and clinical studies. Both original and review articles are welcome. Manuscripts addressing the following issues are of particular interest:

  1. Mechanistic studies of natural product treatments for protecting against ischemic stroke injury by targeting the central nervous system and/or immune system;
  2. Mechanistic studies of natural product treatments for promoting post-stroke brain recovery via modulating neuronal damages and/or CNS/peripheral immune responses such as inhibiting neurodegeneration, neuroinflammation and peripheral immune suppression and promoting neurogenesis;
  3. Investigation of natural compounds in stroke models that account for comorbidity, such as hyperglycemia, hypertension and hyperlipidemia;
  4. Adjunct therapy of natural products with current therapy for stroke treatment;
  5. Potential combination therapy of natural products with other potential treatments, such as stem cells and optogenetic stimulation.

Dr. Hansen Chen
Dr. Qingkun Liu
Guest Editors

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. Pharmaceuticals 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 2900 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

  • stroke
  • natural products
  • natural compounds
  • neuroprotection
  • brain repair
  • comorbidity
  • adjunct therapy

Published Papers (7 papers)

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Editorial

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3 pages, 184 KiB  
Editorial
Natural Products for the Potential Use of Neuroprotective and Neurorestorative Effects in Stroke
by Hansen Chen and Qingkun Liu
Pharmaceuticals 2023, 16(11), 1516; https://doi.org/10.3390/ph16111516 - 25 Oct 2023
Viewed by 735
Abstract
Stroke is the second leading cause of death and the third leading cause of disability worldwide, with limited treatment options [...] Full article
(This article belongs to the Special Issue Natural Products for Potential Use of Neuroprotective and Neurorestorative Effects in Stroke)

Research

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22 pages, 8654 KiB  
Article
A Comparative Study on the Neuroprotective Effect of Geopung-Chunghyuldan on In Vitro Oxygen–Glucose Deprivation and In Vivo Permanent Middle Cerebral Artery Occlusion Models
by Tae-Hoon Park, Han-Gyul Lee, Seung-Yeon Cho, Seong-Uk Park, Woo-Sang Jung, Jung-Mi Park, Chang-Nam Ko, Ki-Ho Cho, Seungwon Kwon and Sang-Kwan Moon
Pharmaceuticals 2023, 16(4), 596; https://doi.org/10.3390/ph16040596 - 15 Apr 2023
Cited by 1 | Viewed by 1394
Abstract
Geopung-Chunghyuldan (GCD), which is a mixture of Chunghyuldan (CD), Radix Salviae Miltiorrhizae, Radix Notoginseng, and Borneolum Syntheticum, is used to treat ischemic stroke in traditional Korean medicine. This study aimed to investigate the effects of GCD and CD on ischemic brain damage using [...] Read more.
Geopung-Chunghyuldan (GCD), which is a mixture of Chunghyuldan (CD), Radix Salviae Miltiorrhizae, Radix Notoginseng, and Borneolum Syntheticum, is used to treat ischemic stroke in traditional Korean medicine. This study aimed to investigate the effects of GCD and CD on ischemic brain damage using in vitro and in vivo stroke models, as well as to elucidate the synergistic effects of GCD against ischemic insult. To study the effect of GCD in an in vitro ischemia model, SH-SY5Y cells were exposed to oxygen–glucose deprivation (OGD). Cell death after 16 h of OGD exposure was measured using the MTT assay and live/dead cell counting methods. An in vivo ischemia mice model was established through permanent middle cerebral artery occlusion (pMCAO). To determine the neuroprotective effect of GCD, it was orally administered immediately and 2 h after pMCAO. The infarct volume was measured through 2,3,5-triphenyltetrazolium chloride staining at 24 h after pMCAO. Compared with the control group, GCD treatment significantly reduced OGD-induced cell death in SH-SY5Y cells; however, CD treatment did not show a significant protective effect. In the pMCAO model, compared with the control group, treatment with GCD and CD significantly and mildly reduced the infarct volume, respectively. Our findings indicate that compared with CD, GCD may allow a more enhanced neuroprotective effect in acute ischemic stroke, indicating a potential synergistic neuroprotective effect. The possibility of GCD as a novel alternative choice for the prevention and treatment of ischemic stroke is suggested. Full article
(This article belongs to the Special Issue Natural Products for Potential Use of Neuroprotective and Neurorestorative Effects in Stroke)
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20 pages, 4253 KiB  
Article
Anethole Pretreatment Modulates Cerebral Ischemia/Reperfusion: The Role of JNK, p38, MMP-2 and MMP-9 Pathways
by Nancy S. Younis and Maged E. Mohamed
Pharmaceuticals 2023, 16(3), 442; https://doi.org/10.3390/ph16030442 - 15 Mar 2023
Cited by 3 | Viewed by 1758
Abstract
Anethole (AN) is one of the major constituents of several plant oils, demonstrating plentiful pharmacological actions. Ischemic stroke is the main cause of morbidity and death worldwide, particularly since ischemic stroke therapeutic choices are inadequate and limited; thus, the development of new therapeutic [...] Read more.
Anethole (AN) is one of the major constituents of several plant oils, demonstrating plentiful pharmacological actions. Ischemic stroke is the main cause of morbidity and death worldwide, particularly since ischemic stroke therapeutic choices are inadequate and limited; thus, the development of new therapeutic options is indispensable. This study was planned to explore the preventive actions of AN in ameliorating cerebral ischemia/reperfusion-induced brain damage and BBB permeability leakage, as well as to explore anethole’s potential mechanisms of action. The proposed mechanisms included modulating JNK and p38 as well as MMP-2 and MMP-9 pathways. Sprague–Dawley male rats were randomly assigned into four groups: sham, middle cerebral artery occlusion (MCAO), AN125 + MCAO, and AN250 + MCAO. Animals in the third and fourth groups were pretreated with AN 125 or 250 mg/kg orally, respectively, for two weeks before performing middle cerebral artery occlusion (MCAO)-induced cerebral ischemic/reperfusion surgery. Animals that experienced cerebral ischemia/reperfusion exhibited amplified infarct volume, Evans blue intensity, brain water content, Fluoro-Jade B-positive cells, severe neurological deficits, and numerous histopathological alterations. MCAO animals exhibited elevated MMP-9 and MMP-2 gene expressions, enzyme activities, augmented JNK, and p38 phosphorylation. On the other hand, pretreatment with AN diminished the infarct volume, Evans blue dye intensity, brain water content, and Fluoro-Jade B-positive cells, improved the neurological score and enhanced histopathological examination. AN effectively lowered MMP-9 and MMP-2 gene expression and enzyme activities and diminished phosphorylated JNK, p38. AN decreased MDA content, amplified GSH/GSSG ratio, SOD, and CAT, decreased the serum and brain tissue homogenate inflammatory cytokines (TNF-α, IL-6, IL-1β), NF-κB, and deterred the apoptotic status. This study revealed the neuroprotective ability of AN against cerebral ischemia/reperfusion in rats. AN boosted blood–brain barrier integrity via modulating MMPs and diminished oxidative stress, inflammation, and apoptosis through the JNK/p38 pathway. Full article
(This article belongs to the Special Issue Natural Products for Potential Use of Neuroprotective and Neurorestorative Effects in Stroke)
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14 pages, 3857 KiB  
Article
Astragaloside VI Ameliorates Post-Stroke Depression via Upregulating the NRG-1-Mediated MEK/ERK Pathway
by Xi Chen, Jiangang Shen, Qing Zhou, Xinchun Jin, Haosheng Liu and Ran Gao
Pharmaceuticals 2022, 15(12), 1551; https://doi.org/10.3390/ph15121551 - 13 Dec 2022
Cited by 9 | Viewed by 1580
Abstract
Background: Post-stroke depression (PSD) has been identified as one of the most commonly occurring complications attributed to stroke. Astragaloside VI (AsVI), which is an active Radix Astragali (AR)-derived compound, has been reported to be a potential drug for post-stroke therapy, but its effects [...] Read more.
Background: Post-stroke depression (PSD) has been identified as one of the most commonly occurring complications attributed to stroke. Astragaloside VI (AsVI), which is an active Radix Astragali (AR)-derived compound, has been reported to be a potential drug for post-stroke therapy, but its effects on PSD and the underlying mechanisms remain uncovered. Methods: In this study, healthy male SD rats underwent a middle cerebral artery occlusion (MCAO) stroke model. To create a PSD model, these rats were then kept in isolated houses and subjected to chronic unpredictable mild stress. The rats were examined every five days for a series of behavioral tests of depression. The antidepressant properties of AsVI were also investigated in vitro in a corticosterone (CORT)-induced major depression model using a CCK-8 assay. The release of neurotransmitters dopamine (DA)/5-hydroxytryptamine (5-HT) was measured using HPLC. The expression of the neurotrophic factor Neuregulin 1 (NRG-1) in rat brain tissues was detected by immunostaining. The protein expression of NRG-1, p-MEK1, and p-ERK1/2 was analyzed utilizing western blotting. Results: AsVI treatment significantly reduced depression-like behaviors in PSD rats and attenuated the CORT-induced apoptotic cell death in neuronal PC-12 cells. Besides, AsVI treatment remarkably prevented the decrease of the levels of DA and 5-HT in the PSD rat brains and in CORT-induced PC-12 cells. Furthermore, AsVI treatment upregulated the NRG-1-mediated MEK/ERK pathway, which is associated with the improvement of PSD. Conclusions: These findings suggest that AsVI could improve PSD at least partially by upregulating NRG-1-mediated MEK/ERK pathway. AsVI could be a novel therapeutic option for treating PSD. Full article
(This article belongs to the Special Issue Natural Products for Potential Use of Neuroprotective and Neurorestorative Effects in Stroke)
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17 pages, 3087 KiB  
Article
Brain Microvascular Endothelial Cell-Derived Exosomes Protect Neurons from Ischemia–Reperfusion Injury in Mice
by Jin Sun, Qing Yuan, Lichen Guo, Guangxu Xiao, Tong Zhang, Bing Liang, Rongmei Yao, Yan Zhu, Yue Li and Limin Hu
Pharmaceuticals 2022, 15(10), 1287; https://doi.org/10.3390/ph15101287 - 19 Oct 2022
Cited by 5 | Viewed by 1914
Abstract
Stroke often results in neurological and neuropsychiatric sequela. Exosomes derived from brain endothelial cells (EC-Exo) protect neurons from hypoxic injury. However, the biological role of exosomes in apoptosis and synaptic plasticity remains unclear. This research aimed to assess whether cerebral microvascular endothelial cells [...] Read more.
Stroke often results in neurological and neuropsychiatric sequela. Exosomes derived from brain endothelial cells (EC-Exo) protect neurons from hypoxic injury. However, the biological role of exosomes in apoptosis and synaptic plasticity remains unclear. This research aimed to assess whether cerebral microvascular endothelial cells inhibit apoptosis and promote synaptic remodeling through exosome-mediated cell–cell interaction after the ischemic attack. The effects of EC-Exo on primary neuronal apoptosis and synapses in oxyglucose deprivation reoxygenation (OGD/R) injury were first assessed in vitro. Animal experiments were performed using C57BL/6J mice, divided into three groups: a sham group, a model (middle cerebral artery occlusion/reperfusion, MCAO/R) group, and an EC-Exo group (tail vein injection of EC-Exo, once/2 days for 14 days) to evaluate the neuromotor and exploratory abilities of mice after MCAO/R. Apoptosis and synaptic protein expression levels were detected. The results demonstrated that EC-Exo inhibited neuronal apoptosis and increased synaptic length after OGD/R. In vivo, EC-Exo not only improved neural motor behavior and increased regional cerebral blood flow (rCBF) in MCAO/R-injured mice but also promoted the expression of synaptic regulatory proteins and inhibited apoptosis in the brain. These results suggest that EC-Exo may provide neuroprotection against stroke by promoting synaptic remodeling and inhibiting apoptosis from protecting neurons. Full article
(This article belongs to the Special Issue Natural Products for Potential Use of Neuroprotective and Neurorestorative Effects in Stroke)
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12 pages, 1744 KiB  
Article
Neuroprotective Effects of an Edible Pigment Brilliant Blue FCF against Behavioral Abnormity in MCAO Rats
by Jingyang Le, Xiao Xiao, Difan Zhang, Yi Feng, Zhuoying Wu, Yuechun Mao, Chenye Mou, Yanfei Xie, Xiaowei Chen, Hao Liu and Wei Cui
Pharmaceuticals 2022, 15(8), 1018; https://doi.org/10.3390/ph15081018 - 18 Aug 2022
Cited by 1 | Viewed by 2195
Abstract
Ischemic stroke leads to hypoxia-induced neuronal death and behavioral abnormity, and is a major cause of death in the modern society. However, the treatments of this disease are limited. Brilliant Blue FCF (BBF) is an edible pigment used in the food industry that [...] Read more.
Ischemic stroke leads to hypoxia-induced neuronal death and behavioral abnormity, and is a major cause of death in the modern society. However, the treatments of this disease are limited. Brilliant Blue FCF (BBF) is an edible pigment used in the food industry that with multiple aromatic rings and sulfonic acid groups in its structure. BBF and its derivatives were proved to cross the blood-brain barrier and have advantages on the therapy of neuropsychiatric diseases. In this study, BBF, but not its derivatives, significantly ameliorated chemical hypoxia-induced cell death in HT22 hippocampal neuronal cell line. Moreover, protective effects of BBF were attributed to the inhibition of the extracellular regulated protein kinase (ERK) and glycogen synthase kinase-3β (GSK3β) pathways as evidenced by Western blotting analysis and specific inhibitors. Furthermore, BBF significantly reduced neurological and behavioral abnormity, and decreased brain infarct volume and cerebral edema induced by middle cerebral artery occlusion/reperfusion (MCAO) in rats. MCAO-induced increase of p-ERK in ischemic penumbra was reduced by BBF in rats. These results suggested that BBF prevented chemical hypoxia-induced otoxicity and MCAO-induced behavioral abnormity via the inhibition of the ERK and GSK3β pathways, indicating the potential use of BBF for treating ischemic stroke Full article
(This article belongs to the Special Issue Natural Products for Potential Use of Neuroprotective and Neurorestorative Effects in Stroke)
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Review

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20 pages, 1344 KiB  
Review
Therapeutic Potential of Chinese Medicine for Endogenous Neurogenesis: A Promising Candidate for Stroke Treatment
by Lin Li, Xiao Li, Rui Han, Meirong Wu, Yaolei Ma, Yuzhao Chen, Han Zhang and Yue Li
Pharmaceuticals 2023, 16(5), 706; https://doi.org/10.3390/ph16050706 - 07 May 2023
Cited by 1 | Viewed by 1868
Abstract
Strokes are a leading cause of morbidity and mortality in adults worldwide. Extensive preclinical studies have shown that neural-stem-cell-based treatments have great therapeutic potential for stroke. Several studies have confirmed that the effective components of traditional Chinese medicine can protect and maintain the [...] Read more.
Strokes are a leading cause of morbidity and mortality in adults worldwide. Extensive preclinical studies have shown that neural-stem-cell-based treatments have great therapeutic potential for stroke. Several studies have confirmed that the effective components of traditional Chinese medicine can protect and maintain the survival, proliferation, and differentiation of endogenous neural stem cells through different targets and mechanisms. Therefore, the use of Chinese medicines to activate and promote endogenous nerve regeneration and repair is a potential treatment option for stroke patients. Here, we summarize the current knowledge regarding neural stem cell strategies for ischemic strokes and the potential effects of these Chinese medicines on neuronal regeneration. Full article
(This article belongs to the Special Issue Natural Products for Potential Use of Neuroprotective and Neurorestorative Effects in Stroke)
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