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The Role of Natural Products in the Treatment of Neuronal Disease

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: closed (31 October 2022) | Viewed by 9839

Special Issue Editor

Dr. Sunoh Kim

E-Mail Website
Guest Editor
Central R&D Center, B&Tech Co., Ltd., Gwangju, Republic of Korea
Interests: electroneurophysiology; neuroreceptors; voltage-dependent calcium channels; neurological diseases; cardiovascular disease; neuropharmacology; molecular biology; natural product; Alzheimer’s disease; obesity; hypertension
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

The nervous system is composed of various nerve cells that perfectly control the human body. Until now, many studies have been reported to discover new drugs that inhibit neuronal cell death and regenerate neuronal cells. However, there are many limitations in treating many neurological diseases, including dementia and depression. In this Special Issue, we would like to examine the application of natural products to control various neurological diseases. For the central nervous system and peripheral nervous system, it is necessary to discover various natural products for nervous system diseases and discuss their applicability as therapeutic agents. Natural products contain various phytochemicals. This diversity can suggest the possibility for multi-function, and also sufficiently discuss the synergistic effect. It is very important research to try a therapeutic approach for diseases occurring in various nerve cells and nervous systems such as cerebral nerve, optic nerve, sensory nerve, and olfactory nerve with natural products. We welcome many Colleagues to discuss neurological disease research using natural products.

Topics include but are not limited to the following:

  • Mechanism of optic nerve damage caused by glaucoma
  • Discovering new drugs that modulate excitatory neurotransmitter receptors
  • Discovering new drugs that modulate inhibitory neurotransmitter receptors
  • Discovering new drugs that regulate ion channels
  • Discovering Pain Control Drugs
  • Discovering new drugs for Alzheimer's disease
  • Discovering new drugs for depression
  • Novel Mechanisms for Nervous System Injury

Dr. Sunoh Kim
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

  • natural products
  • phytochemicals
  • nervous system
  • neuronal cell death
  • neurological diseases
  • dementia
  • depression

Published Papers (4 papers)

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Research

16 pages, 2282 KiB  
Article
A Combination of Rosa Multiflora and Zizyphus Jujuba Enhance Sleep Quality in Anesthesia-Induced Mice
by Sanung Eom, Shinhui Lee, Jiwon Lee, Sung-Oh Sohn, Junho H. Lee and Jaeman Park
Int. J. Mol. Sci. 2022, 23(22), 14177; https://doi.org/10.3390/ijms232214177 - 16 Nov 2022
Cited by 3 | Viewed by 1541
Abstract
Sleep is an essential component of quality of life. The majority of people experience sleep problems that impact their quality of life. Melatonin is currently a representative sleep aid. However, it is classified as a prescription drug in most countries, and consumers cannot [...] Read more.
Sleep is an essential component of quality of life. The majority of people experience sleep problems that impact their quality of life. Melatonin is currently a representative sleep aid. However, it is classified as a prescription drug in most countries, and consumers cannot purchase it to improve their sleep. This sleep induction experiment in mice aimed to identify a natural combination product (NCP) that can create synergistic sleep-promoting effects. Based on the mechanism of action of sleep, we investigated whether phenomenological indicators of sleep quality change according to the intake of NCP. The sleep onset and sleep time of the mice that consumed the NCP found by this study were improved compared to the existing sleep aids. The mean melatonin level in the blood increased by 197% compared to the control. To our knowledge, this is the first study to demonstrate that Rosa multiflora Thunb. (Yeongsil) can promote sleep similarly to Zizyphus jujuba Miller (Sanjoin). The results indicate a preclinical study of NCPs containing Rosa multiflora Thunb and Zizyphus jujuba Miller developed by us showed significant differences in sleep incubation and duration depending on melatonin concentrations. Our results also suggest that increased melatonin concentrations in the blood are likely to improve sleep quality, especially regarding incubation periods. Full article
(This article belongs to the Special Issue The Role of Natural Products in the Treatment of Neuronal Disease)
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21 pages, 2722 KiB  
Article
Long-Term Effect of Porcine Brain Enzyme Hydrolysate Intake on Scopolamine-Induced Memory Impairment in Rats
by Ting Zhang, Min Jung Kim, Min Ju Kim, Xuangao Wu, Hye Jeong Yang, Heng Yuan, Shaokai Huang, Sun Myung Yoon, Keun-Nam Kim and Sunmin Park
Int. J. Mol. Sci. 2022, 23(6), 3361; https://doi.org/10.3390/ijms23063361 - 20 Mar 2022
Cited by 9 | Viewed by 2436
Abstract
No study has revealed the effect of porcine brain enzyme hydrolysate (PBEH) on memory impairment. We aimed to examine the hypothesis that PBEH intake modulates memory deficits and cognitive behavior in scopolamine (SC)-induced amnesia rats, and its mechanism, including gut microbiota changes, was [...] Read more.
No study has revealed the effect of porcine brain enzyme hydrolysate (PBEH) on memory impairment. We aimed to examine the hypothesis that PBEH intake modulates memory deficits and cognitive behavior in scopolamine (SC)-induced amnesia rats, and its mechanism, including gut microbiota changes, was determined. Sprague–Dawley male rats had intraperitoneal injections of SC (2 mg/kg body weight/day) at 30 min after daily feeding of casein (MD-control), PBEH (7 mg total nitrogen/mL) at 0.053 mL (Low-PBEH), 0.159 mL (Medium-PBEH), 0.478 mL (High-PBEH), or 10 mg donepezil (Positive-control) per kilogram body weight per day through a feeding needle for six weeks. The Normal-control rats had casein feeding without SC injection. PBEH dose-dependently protected against memory deficits determined by passive avoidance test, Y-maze, water-maze, and novel object recognition test in SC-induced rats compared to the MD-control. The High-PBEH group had a similar memory function to the Positive-control group. Systemic insulin resistance determined by HOMA-IR was lower in the PBEH groups than in the Normal-control but not the Positive-control. In parallel with systemic insulin resistance, decreased cholesterol and increased glycogen contents in the hippocampus in the Medium-PBEH and High-PBEH represented reduced brain insulin resistance. PBEH intake prevented the increment of serum TNF-α and IL-1β concentrations in the SC-injected rats. Hippocampal lipid peroxide and TNF-α contents and mRNA TNF-α and IL-1β expression were dose-dependently reduced in PBEH and Positive-control. PBEH decreased the hippocampal acetylcholinesterase activity compared to the MD-control, but not as much as the Positive-control. PBEH intake increased the α-diversity of the gut microbiota compared to the MD-control, and the gut microbiota community was separated from MD-control. In metagenome function analysis, PBEH increased the energy metabolism-related pathways of the gut microbiota, including citric acid cycle, oxidative phosphorylation, glycolysis, and amino acid metabolism, which were lower in the MD-control than the Normal-control. In conclusion, alleviated memory deficit by PBEH was associated potentially with not only reducing acetylcholinesterase activity but also improving brain insulin resistance and neuroinflammation potentially through modulating gut microbiota. PBEH intake (1.5–4.5 mL of 7 mg total nitrogen/mL for human equivalent) can be a potential therapeutic agent for improving memory impairment. Full article
(This article belongs to the Special Issue The Role of Natural Products in the Treatment of Neuronal Disease)
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18 pages, 4567 KiB  
Article
Bee Venom Activates the Nrf2/HO-1 and TrkB/CREB/BDNF Pathways in Neuronal Cell Responses against Oxidative Stress Induced by Aβ1–42
by Cong Duc Nguyen, Jaehee Yoo, Sun-Young Hwang, Sung-Young Cho, Myeonghun Kim, Hyemin Jang, Kyoung Ok No, Jeong Cheol Shin, Jae-Hong Kim and Gihyun Lee
Int. J. Mol. Sci. 2022, 23(3), 1193; https://doi.org/10.3390/ijms23031193 - 21 Jan 2022
Cited by 12 | Viewed by 3488
Abstract
Honeybee venom has recently been considered an anti-neurodegenerative agent, primarily due to its anti-inflammatory effects. The natural accumulation of amyloid-beta (Aβ) in the brain is reported to be the natural cause of aging neural ability downfall, and oxidative stress is the main route [...] Read more.
Honeybee venom has recently been considered an anti-neurodegenerative agent, primarily due to its anti-inflammatory effects. The natural accumulation of amyloid-beta (Aβ) in the brain is reported to be the natural cause of aging neural ability downfall, and oxidative stress is the main route by which Aβ ignites its neural toxicity. Anti-neural oxidative stress is considered an effective approach for neurodegenerative therapy. To date, it is unclear how bee venom ameliorates neuronal cells in oxidative stress induced by Aβ. Here, we evaluated the neuroprotective effect of bee venom on Aβ-induced neural oxidative stress in both HT22 cells and an animal model. Our results indicate that bee venom protected HT22 cells against apoptosis induced by Aβ1–42. This protective effect was explained by the increased nuclear translocation of nuclear factor erythroid 2-like 2 (Nrf2), consequently upregulating the production of heme oxygenase-1 (HO-1), a critical cellular instinct antioxidant enzyme that neutralizes excessive oxidative stress. Furthermore, bee venom treatment activated the tropomyosin-related kinase receptor B (TrkB)/cAMP response element-binding (CREB)/brain-derived neurotrophic factor (BDNF), which is closely related to the promotion of cellular antioxidant defense and neuronal functions. A mouse model with cognitive deficits induced by Aβ1–42 intracerebroventricular (ICV) injections was also used. Bee venom enhanced animal cognitive ability and enhanced neural cell genesis in the hippocampal dentate gyrus region in a dose-dependent manner. Further analysis of animal brain tissue and serum confirmed that bee venom reduced oxidative stress, cholinergic system activity, and intercellular neurotrophic factor regulation, which were all adversely affected by Aβ1–42. Our study demonstrates that bee venom exerts antioxidant and neuroprotective actions against neural oxidative stress caused by Aβ1–42, thereby promoting its use as a therapeutic agent for neurodegenerative disorders. Full article
(This article belongs to the Special Issue The Role of Natural Products in the Treatment of Neuronal Disease)
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13 pages, 1519 KiB  
Article
Hydroxy Pentacyclic Triterpene Acid, Kaempferol, Inhibits the Human 5-Hydroxytryptamine Type 3A Receptor Activity
by Shinhui Lee, Hee-Soo Seol, Sanung Eom, Jaeeun Lee, Chaelin Kim, Jong-Hwan Park, Tae-Hwan Kim and Junho H. Lee
Int. J. Mol. Sci. 2022, 23(1), 544; https://doi.org/10.3390/ijms23010544 - 4 Jan 2022
Cited by 12 | Viewed by 1717
Abstract
Monoamine serotonin is a major neurotransmitter that acts on a wide range of central nervous system and peripheral nervous system functions and is known to have a role in various processes. Recently, it has been found that 5-HT is involved in cognitive and [...] Read more.
Monoamine serotonin is a major neurotransmitter that acts on a wide range of central nervous system and peripheral nervous system functions and is known to have a role in various processes. Recently, it has been found that 5-HT is involved in cognitive and memory functions through interaction with cholinergic pathways. The natural flavonoid kaempferol (KAE) extracted from Cudrania tricuspidata is a secondary metabolite of the plant. Recently studies have confirmed that KAE possesses a neuroprotective effect because of its strong antioxidant activity. It has been confirmed that KAE is involved in the serotonergic pathway through an in vivo test. However, these results need to be confirmed at the molecular level, because the exact mechanism that is involved in such effects of KAE has not yet been elucidated. Therefore, the objective of this study is to confirm the interaction of KAE with 5-HT3A through electrophysiological studies at the molecular level using KAE extracted from Cudrania tricuspidata. This study confirmed the interaction between 5-HT3A and KAE at the molecular level. KAE inhibited 5-HT3A receptors in a concentration-dependent and voltage-independent manner. Site-directed mutagenesis and molecular-docking studies confirmed that the binding sites D177 and F199 are the major binding sites of human 5-HT3A receptors of KAE. Full article
(This article belongs to the Special Issue The Role of Natural Products in the Treatment of Neuronal Disease)
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