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Animal Models of Human Diseases and Their Potential Therapies of Natural Products or Pure Components

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Natural Products Chemistry".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 17164

Special Issue Editors


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Guest Editor
Department of Food Science and Biotechnology, Da-Yeh University, Dacun, Taiwan
Interests: healthy foods; experimental zoology; Chinese herbal medicine research; animal models of human diseases; natural biological activity

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Guest Editor
Department of Biomedical Sciences, Chung Shan Medical University, Taichung, Taiwan
Interests: developmental biology; gene transfer; molecular reproduction; embryonic development; animal models of human diseases

Special Issue Information

Dear Colleagues,

This Special Issue collects original research articles and comprehensive reviews. It focuses on results from laboratory animals but not from animal cells or human patients. Research and reviews with the following topics are welcome:

  1. Comprehensive reviews focusing on summaries or comparisons of the therapeutic effect of a category of compounds, components, natural products, or herbal extracts on a specific animal model of human disease;
  2. Original research articles using a novel, modified, or well-established animal model of human disease to screen or test potential drugs, natural products, or herbal extracts, showing the molecule mechanisms of their functions.

Prof. Dr. Ming-Shiun Tsai
Prof. Dr. Sue-Hong Wang
Guest Editors

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Keywords

  • laboratory animals
  • animal models
  • herbal extracts
  • natural products
  • pure compounds
  • drug screening
  • drug testing
  • molecule mechanisms

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Published Papers (3 papers)

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Research

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12 pages, 2163 KiB  
Article
Curcuma phaeocaulis Inhibits NLRP3 Inflammasome in Macrophages and Ameliorates Nanoparticle-Induced Airway Inflammation in Mice
by Yeon-Ju Nam, Jiwon Choi, Jong Suk Lee, Changon Seo, Gyeongbeen Lee, Youngsu Lee, Jin Kyu Kim, Pansoo Kim, Jeong Ju Lim, Hyeon-Son Choi and Yongmun Choi
Molecules 2022, 27(7), 2101; https://doi.org/10.3390/molecules27072101 - 24 Mar 2022
Cited by 9 | Viewed by 2440
Abstract
The activation of NLRP3 results in the assembly of inflammasome that regulates caspase-1 activation and the subsequent secretion of bioactive interleukin (IL)-1β. Excessive activation of the NLRP3 inflammasome is mechanistically linked to diverse pathophysiological conditions, including airway inflammation. Here, we discovered that Curcuma [...] Read more.
The activation of NLRP3 results in the assembly of inflammasome that regulates caspase-1 activation and the subsequent secretion of bioactive interleukin (IL)-1β. Excessive activation of the NLRP3 inflammasome is mechanistically linked to diverse pathophysiological conditions, including airway inflammation. Here, we discovered that Curcuma phaeocaulis can suppress caspase-1 activation and processing of pro-IL-1β into mature cytokine in macrophages stimulated with NLRP3 inflammasome activators, such as SiO2 or TiO2 nanoparticles. Furthermore, in the bronchoalveolar lavage fluids of animals administered the nanoparticles, the in vitro effects of C. phaeocaulis translated into a decrease in IL-1β levels and cell infiltration. Demethoxycurcumin (DMC) and curcumin were found to be responsible for the inflammasome inhibitory activity of C. phaeocaulis. Interestingly, in contrast to the previously reported higher antioxidant- and NFκB-inhibitory activities of curcumin, DMC exhibited approximately two-fold stronger potency than curcumin against nanoparticle induced activation of NLRP3 inflammasome. In the light of these results, both compounds seem to act independently of their antioxidant- and NFκB-inhibitory properties. Although how C. phaeocaulis inhibits nanoparticle-activated NLRP3 inflammasome remains to be elucidated, our results provide a basis for further research on C. phaeocaulis extract as an anti-inflammatory agent for the treatment of disorders associated with excessive activation of NLRP3 inflammasome. Full article
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Review

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23 pages, 1625 KiB  
Review
Flavonoids in Treatment of Chronic Kidney Disease
by Yi-Ling Cao, Ji-Hong Lin, Hans-Peter Hammes and Chun Zhang
Molecules 2022, 27(7), 2365; https://doi.org/10.3390/molecules27072365 - 6 Apr 2022
Cited by 35 | Viewed by 7175
Abstract
Chronic kidney disease (CKD) is a progressive systemic disease, which changes the function and structure of the kidneys irreversibly over months or years. The final common pathological manifestation of chronic kidney disease is renal fibrosis and is characterized by glomerulosclerosis, tubular atrophy, and [...] Read more.
Chronic kidney disease (CKD) is a progressive systemic disease, which changes the function and structure of the kidneys irreversibly over months or years. The final common pathological manifestation of chronic kidney disease is renal fibrosis and is characterized by glomerulosclerosis, tubular atrophy, and interstitial fibrosis. In recent years, numerous studies have reported the therapeutic benefits of natural products against modern diseases. Substantial attention has been focused on the biological role of polyphenols, in particular flavonoids, presenting broadly in plants and diets, referring to thousands of plant compounds with a common basic structure. Evidence-based pharmacological data have shown that flavonoids play an important role in preventing and managing CKD and renal fibrosis. These compounds can prevent renal dysfunction and improve renal function by blocking or suppressing deleterious pathways such as oxidative stress and inflammation. In this review, we summarize the function and beneficial properties of common flavonoids for the treatment of CKD and the relative risk factors of CKD. Full article
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12 pages, 295 KiB  
Review
A Comparison of the Gene Expression Profiles of Non-Alcoholic Fatty Liver Disease between Animal Models of a High-Fat Diet and Methionine-Choline-Deficient Diet
by Mohammed Abdullah Alshawsh, Abdulsamad Alsalahi, Salah Abdalrazak Alshehade, Sultan Ayesh Mohammed Saghir, Ahmad Faheem Ahmeda, Raghdaa Hamdan Al Zarzour and Ayman Moawad Mahmoud
Molecules 2022, 27(3), 858; https://doi.org/10.3390/molecules27030858 - 27 Jan 2022
Cited by 45 | Viewed by 6475
Abstract
Non-alcoholic fatty liver disease (NAFLD) embraces several forms of liver disorders involving fat disposition in hepatocytes ranging from simple steatosis to the severe stage, namely, non-alcoholic steatohepatitis (NASH). Recently, several experimental in vivo animal models for NAFLD/NASH have been established. However, no reproducible [...] Read more.
Non-alcoholic fatty liver disease (NAFLD) embraces several forms of liver disorders involving fat disposition in hepatocytes ranging from simple steatosis to the severe stage, namely, non-alcoholic steatohepatitis (NASH). Recently, several experimental in vivo animal models for NAFLD/NASH have been established. However, no reproducible experimental animal model displays the full spectrum of pathophysiological, histological, molecular, and clinical features associated with human NAFLD/NASH progression. Although methionine-choline-deficient (MCD) diet and high-fat diet (HFD) models can mimic histological and metabolic abnormalities of human disease, respectively, the molecular signaling pathways are extremely important for understanding the pathogenesis of the disease. This review aimed to assess the differences in gene expression patterns and NAFLD/NASH progression pathways among the most common dietary animal models, i.e., HFD- and MCD diet-fed animals. Studies showed that the HFD and MCD diet could induce either up- or downregulation of the expression of genes and proteins that are involved in lipid metabolism, inflammation, oxidative stress, and fibrogenesis pathways. Interestingly, the MCD diet model could spontaneously develop liver fibrosis within two to four weeks and has significant effects on the expression of genes that encode proteins and enzymes involved in the liver fibrogenesis pathway. However, such effects in the HFD model were found to occur after 24 weeks with insulin resistance but appear to cause less severe fibrosis. In conclusion, assessing the abnormal gene expression patterns caused by different diet types provides valuable information regarding the molecular mechanisms of NAFLD/NASH and predicts the clinical progression of the disease. However, expression profiling studies concerning genetic variants involved in the development and progression of NAFLD/NASH should be conducted. Full article
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