Natural Products in Health Promotion and Disease Prevention 2024

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

Deadline for manuscript submissions: 20 February 2025 | Viewed by 4606

Special Issue Editors


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Guest Editor
Department of Biochemistry, Federal University of Santa Catarina, Florianópolis, SC, Brazil
Interests: redox mechanisms in biological systems; environmental toxicology and health; molecular mechanisms of disease; chemical stressor toxicity; reproductive endocrinology and toxicology; drug discovery and development; interdisciplinary approaches in biosciences
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Special Issue Information

Dear Colleagues,

Celebrating its 20th year, Pharmaceuticals is delighted to invite scientists to contribute articles and literature reviews on the impact and potential of natural products in health promotion and disease prevention. This Special Issue aims to explore the intersection between natural products and pharmaceutical science, highlighting recent discoveries and innovations. Natural products, encompassing a wide range of biological substances, have been used for health enhancement and disease treatment since ancient times. With the advancement of modern science, these products are being reevaluated, offering therapeutic benefits. This Special Issue seeks to gather research on the efficacy, safety, mechanisms of action and therapeutic potential of natural products. We are particularly interested in studies addressing the following themes: identification and characterization of new bioactive compounds; molecular mechanisms by which natural products influence health and disease; clinical studies testing the efficacy and safety of natural products; synergies between different natural compounds; and the regulatory and ethical implications of using natural products as nutraceuticals. This Special Issue is expected to provide a comprehensive and up-to-date overview of advancements in natural product research, encouraging discussion and collaboration among scientists, health professionals and policy-makers.

Dr. Marco Alves
Prof. Dr. Ariane Zamoner
Guest Editors

Manuscript Submission Information

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Keywords

  • natural products
  • nutraceuticals
  • bioactive compounds
  • traditional medicine
  • drug discovery

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Published Papers (4 papers)

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Research

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16 pages, 8121 KiB  
Article
Mulberry Twig Alkaloids Improved the Progression of Metabolic-Associated Fatty Liver Disease in High-Fat Diet-Induced Obese Mice by Regulating the PGC1α/PPARα and KEAP1/NRF2 Pathways
by Mengqing Zhang, Chengcheng Guo, Zonglin Li, Xiaoling Cai, Xin Wen, Fang Lv, Chu Lin and Linong Ji
Pharmaceuticals 2024, 17(10), 1287; https://doi.org/10.3390/ph17101287 - 27 Sep 2024
Viewed by 815
Abstract
Background/Objectives: Metabolic-associated fatty liver disease (MAFLD) is one of the most common liver disorders associated with obesity and metabolic syndrome, and poses a significant global health burden with limited effective treatments. The aim of this study was to assess the protective effects [...] Read more.
Background/Objectives: Metabolic-associated fatty liver disease (MAFLD) is one of the most common liver disorders associated with obesity and metabolic syndrome, and poses a significant global health burden with limited effective treatments. The aim of this study was to assess the protective effects of mulberry twig alkaloids (SZ-A) on MAFLD and to further investigate the underlying mechanisms including the specific targets or pathways. Methods: Diet-induced obesity (DIO) and normal mouse models were established by feeding C57Bl/6J mice with a high-fat diet (HFD) or common diet for 12 weeks. SZ-A, dapagliflozin, and placebo were administered to corresponding mouse groups for 8 weeks. Data of fasting blood glucose, glucose tolerance, insulin tolerance, and the body weight of mice were collected at the baseline and termination of the experiment. Serum liver enzymes and lipids were measured by ELISA. Western blotting, qPCR, and pathological section staining were implemented to evaluate the degrees of liver steatosis, fibrosis, and oxidative stress in mice. Results: In DIO mouse models, high-dose SZ-A (800 mg/kg/d) treatment significantly inhibited HFD-induced weight gain, improved insulin tolerance, and reduced serum alanine aminotransferase, total cholesterol, and triglyceride levels compared with placebo. In DIO mice, SZ-A could alleviate the pathological changes of hepatic steatosis and fibrosis compared with placebo. Lipid catabolism and antioxidant stress-related proteins were significantly increased in the livers of the high-dose SZ-A group (p < 0.05). Inhibition of PGC1α could inhibit the function of SZ-A to enhance lipid metabolism in hepatocytes. PGC1α might interact with NRF2 to exert MAFLD-remedying effects. Conclusions: By regulating the expression of PGC1α and its interacting KEAP1/NRF2 pathway in mouse liver cells, SZ-A played important roles in regulating lipid metabolism, inhibiting oxidative stress, and postponing liver fibrosis in mice with MAFLD. Full article
(This article belongs to the Special Issue Natural Products in Health Promotion and Disease Prevention 2024)
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17 pages, 9794 KiB  
Article
Chemical Compositions of Lianqiao (Forsythia suspensa) Extracts and Their Potential Health Benefits
by Boyan Gao, Hanshu Zhu, Zhihao Liu, Xiaohua He, Jianghao Sun, Yanfang Li, Xianli Wu, Pamela Pehrsson, Yaqiong Zhang, Yuanhang Yao and Liangli Yu
Pharmaceuticals 2024, 17(6), 740; https://doi.org/10.3390/ph17060740 - 6 Jun 2024
Cited by 2 | Viewed by 861
Abstract
This study evaluated the fruits of Forsythia suspensa (Lianqiao), an important economic crop, for the chemical components of its water and ethanol extracts, inhibitory effects on SARS-CoV-2 virus spike protein binding to ACE2, inhibition of ACE2 activity, and capacity to scavenge free radicals. [...] Read more.
This study evaluated the fruits of Forsythia suspensa (Lianqiao), an important economic crop, for the chemical components of its water and ethanol extracts, inhibitory effects on SARS-CoV-2 virus spike protein binding to ACE2, inhibition of ACE2 activity, and capacity to scavenge free radicals. A total of 42 compounds were tentatively identified in the extracts via HPLC-MS/MS analysis. The water extract showed a greater ACE2 inhibition but a weaker inhibition on SARS-CoV-2 spike protein binding to ACE2 than the ethanol extract on a per-botanical-weight-concentration basis. The phenolic content was found to be greater in the water extract at 45.19 mg GAE/g dry botanical weight than in the ethanol extract (6.89 mg GAE/g dry botanical). Furthermore, the water extract had greater scavenging capacities against HO, DPPH, and ABTS●+ at 448.48, 66.36, and 121.29 µmol TE/g dry botanical, respectively, as compared to that of the ethanol extract (154.04, 3.55, and 33.83 µmol TE/g dry botanical, respectively). These results warrant further research into, and the development of, the potential COVID-19-preventive applications of Lianqiao and its extracts. Full article
(This article belongs to the Special Issue Natural Products in Health Promotion and Disease Prevention 2024)
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18 pages, 2975 KiB  
Article
Barbaloin Protects Pentylenetetrazol-Induced Cognitive Deficits in Rodents via Modulation of Neurotransmitters and Inhibition of Oxidative-Free-Radicals-Led Inflammation
by Ahmad Essam Altyar, Muhammad Afzal, Nehmat Ghaboura, Khalid Saad Alharbi, Sattam Khulaif Alenezi, Nadeem Sayyed and Imran Kazmi
Pharmaceuticals 2024, 17(6), 699; https://doi.org/10.3390/ph17060699 - 28 May 2024
Viewed by 1031
Abstract
Background: Epilepsy is defined by an excessive level of activity in the neurons and coordinated bursts of electrical activity, resulting in the occurrence of seizure episodes. The precise cause of epileptogenesis remains uncertain; nevertheless, the etiology of epilepsy may involve neuroinflammation, oxidative stress, [...] Read more.
Background: Epilepsy is defined by an excessive level of activity in the neurons and coordinated bursts of electrical activity, resulting in the occurrence of seizure episodes. The precise cause of epileptogenesis remains uncertain; nevertheless, the etiology of epilepsy may involve neuroinflammation, oxidative stress, and malfunction of the neurotransmitter system. Objective: The goal of this investigation was to assess barbaloin’s protective properties with respect to pentylenetetrazol (PTZ)-)-induced cognitive deficits in rats via antioxidative, anti-inflammatory, and neurotransmitter-modulating effects. Methods: Wistar rats were subjected to PTZ [40 mg/kg (i.p.)], which induced cognitive decline. Behavior assessment using a kindling score, open-field test (OFT), novel object recognition test (NORT), and assays for superoxide dismutase (SOD), reduced glutathione (GSH), catalase (CAT), malondialdehyde (MDA), acetylcholinesterase (AChE), caspase-3, nitric oxide (NO), interleukins-1β (IL-1β), tumor necrosis factor-α (TNF-α), IL-6, nuclear factor kappa-B (NF-κB), Bcl-2 and Bax, and neurotransmitter levels [GABA, DA, NE, and serotonin (5-HT)] were performed. Results: The treatment of rats with barbaloin resulted in behavior improvement and significant changes in the levels of GSH, SOD, CAT, MDA, AChE, NO, IL-6, IL-1β, TNF-α, NF-κB, caspase-3, Bcl-2, and Bax compared to the PTZ control group. Barbaloin treatment resulted in notable changes in neurotransmitter levels (GABA, NE, 5-HT, DA) compared to the PTZ group. Conclusions: The ongoing study has gathered evidence indicating that the injection of barbaloin has resulted in significant improvements in cognitive performance in rats. This is achieved by inhibiting oxidative stress, enhancing the activity of natural antioxidant enzymes, reducing cytokine levels, and increasing the levels of neurotransmitters in the brain. These results were detected in comparison to a PTZ control and can be attributed to the potent anti-inflammatory and antioxidant capabilities of barbaloin, which could be linked to its neuroprotective properties. Barbaloin may potentially increase cognitive decline and boost neuronal survival by altering the expression of Bax, caspase-3, Bcl-2. Full article
(This article belongs to the Special Issue Natural Products in Health Promotion and Disease Prevention 2024)
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Review

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24 pages, 1688 KiB  
Review
Unlocking Cholesterol Metabolism in Metabolic-Associated Steatotic Liver Disease: Molecular Targets and Natural Product Interventions
by Xiaoxiao Li and Meng Li
Pharmaceuticals 2024, 17(8), 1073; https://doi.org/10.3390/ph17081073 - 15 Aug 2024
Viewed by 1285
Abstract
Metabolic-associated steatotic liver disease (MASLD), the hepatic manifestation of metabolic syndrome, represents a growing global health concern. The intricate pathogenesis of MASLD, driven by genetic, metabolic, epigenetic, and environmental factors, leads to considerable clinical variability. Dysregulation of hepatic lipid metabolism, particularly cholesterol homeostasis, [...] Read more.
Metabolic-associated steatotic liver disease (MASLD), the hepatic manifestation of metabolic syndrome, represents a growing global health concern. The intricate pathogenesis of MASLD, driven by genetic, metabolic, epigenetic, and environmental factors, leads to considerable clinical variability. Dysregulation of hepatic lipid metabolism, particularly cholesterol homeostasis, is a critical factor in the progression of MASLD and its more severe form, metabolic dysfunction-associated steatohepatitis (MASH). This review elucidates the multifaceted roles of cholesterol metabolism in MASLD, focusing on its absorption, transportation, biosynthesis, efflux, and conversion. We highlight recent advancements in understanding these processes and explore the therapeutic potential of natural products such as curcumin, berberine, and resveratrol in modulating cholesterol metabolism. By targeting key molecular pathways, these natural products offer promising strategies for MASLD management. Finally, this review also covers the clinical studies of natural products in MASLD, providing new insights for future research and clinical applications. Full article
(This article belongs to the Special Issue Natural Products in Health Promotion and Disease Prevention 2024)
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