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Cells
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Protective and Therapeutic Potential of Natural Products and Their Bioactive...
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Protective and Therapeutic Potential of Natural Products and Their Bioactive Compounds in the Inflammatory Disorders of Nervous System

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: closed (1 December 2021) | Viewed by 17531

Special Issue Editor

Prof. Dr. Maria Antonietta Panaro

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Guest Editor
Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, Bari, Italy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Natural products, derived from plants and /or animals, together with their bioactive compounds have been intensively investigated and gained a lot of interest for their therapeutic potential for various diseases, including neuroinflammatory diseases. Neuroinflammation, which is involved in various inflammatory cascades in nervous tissues, can result in persistent and chronic apoptotic neuronal cell death and programmed cell death, triggering various degenerative disorders of the central nervous system. Natural compounds have been extensively studied regarding their antioxidant and anti-inflammatory activities and the broad spectrum of pharmacological or biological activities has made them suitable candidates for the treatment of neurodegenerative diseases. However, the physicochemical properties of natural products are not overlapped to those of drugs and a series of problems concerning their stability and neuroavailability must be overcome to be accepted as effective therapies.

This special issue focuses on the various established activities of natural products and their bioactive compounds, in in vitro and in vivo preclinical models, and their potential neurotherapeutic applications.

Prof. Dr. Maria Antonietta Panaro
Guest Editor

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Keywords

  • inflammation
  • neurodegeneration
  • natural compounds
  • therapy
  • drug target
  • cell signalling
  • cells of nervous system

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Published Papers (3 papers)

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Research

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16 pages, 6650 KiB  
Article
Cycloastragenol, a Triterpenoid Saponin, Regulates Oxidative Stress, Neurotrophic Dysfunctions, Neuroinflammation and Apoptotic Cell Death in Neurodegenerative Conditions
by Muhammad Ikram, Myeung Hoon Jo, Kyonghwan Choe, Amjad Khan, Sareer Ahmad, Kamran Saeed, Min Woo Kim and Myeong Ok Kim
Cells 2021, 10(10), 2719; https://doi.org/10.3390/cells10102719 - 11 Oct 2021
Cited by 25 | Viewed by 4253
Abstract
Here, we have unveiled the effects of cycloastragenol against Aβ (Amyloid-beta)-induced oxidative stress, neurogenic dysfunction, activated mitogen-activated protein (MAP) kinases, and mitochondrial apoptosis in an Aβ-induced mouse model of Alzheimer’s disease (AD). The Aβ-induced mouse model was developed by the stereotaxic injection of [...] Read more.
Here, we have unveiled the effects of cycloastragenol against Aβ (Amyloid-beta)-induced oxidative stress, neurogenic dysfunction, activated mitogen-activated protein (MAP) kinases, and mitochondrial apoptosis in an Aβ-induced mouse model of Alzheimer’s disease (AD). The Aβ-induced mouse model was developed by the stereotaxic injection of amyloid-beta (5 μg/mouse/intracerebroventricular), and cycloastragenol was given at a dose of 20 mg/kg/day/p.o for 6 weeks daily. For the biochemical analysis, we used immunofluorescence and Western blotting. Our findings showed that the injection of Aβ elevated oxidative stress and reduced the expression of neurogenic markers, as shown by the reduced expression of brain-derived neurotrophic factor (BDNF) and the phosphorylation of its specific receptor tropomyosin receptor kinase B (p-TrKB). In addition, there was a marked reduction in the expression of NeuN (neuronal nuclear protein) in the Aβ-injected mice brains (cortex and hippocampus). Interestingly, the expression of Nrf2 (nuclear factor erythroid 2–related factor 2), HO-1 (heme oxygenase-1), p-TrKB, BDNF, and NeuN was markedly enhanced in the Aβ + Cycloastragenol co-treated mice brains. We have also evaluated the expressions of MAP kinases such as phospho c-Jun-N-terminal kinase (p-JNK), p-38, and phospho-extracellular signal-related kinase (ERK1/2) in the experimental groups, which suggested that the expression of p-JNK, p-P-38, and p-Erk were significantly upregulated in the Aβ-injected mice brains; interestingly, these markers were downregulated in the Aβ + Cycloastragenol co-treated mice brains. We also checked the expression of activated microglia and inflammatory cytokines, which showed that cycloastragenol reduced the activated microglia and inflammatory cytokines. Moreover, we evaluated the effects of cycloastragenol against mitochondrial apoptosis and memory dysfunctions in the experimental groups. The findings showed significant regulatory effects against apoptosis and memory dysfunction as revealed by the Morris water maze (MWM) test. Collectively, the findings suggested that cycloastragenol regulates oxidative stress, neurotrophic processes, neuroinflammation, apoptotic cell death, and memory impairment in the mouse model of AD. Full article
(This article belongs to the Special Issue Protective and Therapeutic Potential of Natural Products and Their Bioactive Compounds in the Inflammatory Disorders of Nervous System)
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Review

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26 pages, 3085 KiB  
Review
Can We Use Ginkgo biloba Extract to Treat Alzheimer’s Disease? Lessons from Preclinical and Clinical Studies
by Liming Xie, Qi Zhu and Jiahong Lu
Cells 2022, 11(3), 479; https://doi.org/10.3390/cells11030479 - 29 Jan 2022
Cited by 33 | Viewed by 8201
Abstract
(1) Background: Ginkgo biloba extract (GBE) has been widely used to treat central nervous system and cardiovascular diseases. Accumulating evidence has revealed the therapeutic potential of GBE against Alzheimer's disease (AD); however, no systematic evaluation has been performed; (2) Methods: a total of [...] Read more.
(1) Background: Ginkgo biloba extract (GBE) has been widely used to treat central nervous system and cardiovascular diseases. Accumulating evidence has revealed the therapeutic potential of GBE against Alzheimer's disease (AD); however, no systematic evaluation has been performed; (2) Methods: a total of 17 preclinical studies and 20 clinical trials assessing the therapeutic effects of GBE against AD were identified from electronic databases. The data in the reports were extracted to conduct a meta-analysis of the AD-related pathological features or symptoms; (3) Results: For the preclinical reports, 45 animals treated with GBE, in six studies, were subjected to cognitive function assessments by the Morris water maze. GBE was shown to reduce the escape latencies in several studies, in both rats and mice (I2 > 70%, p < 0.005). For the clinical trials, eight trials, including 2100 individuals, were conducted. The results show that GBE improved the SKT and ADAS-Cog scores in early-stage AD patients after high doses and long-term administration; (4) Conclusions: GBE displayed generally consistent anti-AD effects in animal experiments, and it might improve AD symptoms in early-stage AD patients after high doses and long-term administration. A lack of sample size calculations and the poor quality of the methods are two obvious limitations of the studies. Nevertheless, the preclinical and clinical data suggest that further large-scale clinical trials may be needed in order to examine the effects of long-term GEB administration on early-stage AD. Full article
(This article belongs to the Special Issue Protective and Therapeutic Potential of Natural Products and Their Bioactive Compounds in the Inflammatory Disorders of Nervous System)
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19 pages, 4695 KiB  
Review
Ferulic Acid in Animal Models of Alzheimer’s Disease: A Systematic Review of Preclinical Studies
by Er-Jin Wang, Ming-Yue Wu and Jia-Hong Lu
Cells 2021, 10(10), 2653; https://doi.org/10.3390/cells10102653 - 5 Oct 2021
Cited by 28 | Viewed by 4334
Abstract
Alzheimer’s disease (AD) is a neurodegenerative disease with a high incidence in the elderly. Many preclinical studies show that a natural product, ferulic acid (FA), displays neuroprotective effects in AD models. This review aims to systematically review and meta-analyze published pre-clinical researches about [...] Read more.
Alzheimer’s disease (AD) is a neurodegenerative disease with a high incidence in the elderly. Many preclinical studies show that a natural product, ferulic acid (FA), displays neuroprotective effects in AD models. This review aims to systematically review and meta-analyze published pre-clinical researches about the effects, mechanism, and clinical prospects of FA in the treatment of AD. According to the pre-determined search strategy and inclusion criteria, a total of 344 animals in 12 papers were included in the meta-analysis. We used the fixed effects model to analyze data and I2 and p values to indicate heterogeneity. Results show that FA treatment can effectively improve rodents’ spatial memory ability in MWM and Y maze experiments (I2 ≥ 70, p < 0.005), and reduce the deposition of Aβ in the brains of various model animals (I2 ≥ 50, p < 0.005). The potential mechanisms include anti-amyloidogenesis, anti-inflammation, anti-oxidation, mitochondrial protection, and inhibition of apoptosis. In conclusion, we systematically review and meta-analyze the literature reporting the effects of FA treatment on AD rodent models and solidify the benefits of FA in reducing Aβ deposition and improving memory in preclinical experiments. We also point out the limitations in the current research design and provide a strategy for the production research of FA in the future. Full article
(This article belongs to the Special Issue Protective and Therapeutic Potential of Natural Products and Their Bioactive Compounds in the Inflammatory Disorders of Nervous System)
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