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9.6
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Marine Drugs
Special Issues
Zebrafish Models in Marine Drug Discovery
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Zebrafish Models in Marine Drug Discovery

A special issue of Marine Drugs (ISSN 1660-3397). This special issue belongs to the section "Marine Pharmacology".

Deadline for manuscript submissions: 30 April 2025 | Viewed by 2564

Special Issue Editors

Dr. Xiaobin Li

E-Mail Website
Guest Editor
Biology Institute, Qilu University of Technology (Shandong Academy of Sciences), Jinan 250103, China
Interests: marine natural products; cardiovascular activity; zebrafish models; marine phospholipids
Dr. Yun Zhang

E-Mail Website
Guest Editor
Biology Institute, Qilu University of Technology (Shandong Academy of Sciences), Jinan 250103, China
Interests: marine drug; marine sponge; marine sponge symbiotic fungus

Special Issue Information

Dear Colleagues,

Marine organisms are a vital source of lead compounds for drugs. Bioactivity evaluation is an indispensable step in drug discovery. However, evaluating the activity of marine natural products is often limited by their low content.

Zebrafish have the unique advantages of a short reproductive cycle, in vitro embryo development, overall embryo transparency, high genetic similarity to humans, easy maintenance, and low cost. As an ideal vertebrate model, zebrafish are widely used in screening the bioactivity of natural active compounds. Furthermore, activity evaluation using zebrafish models requires minimal sample volumes, making them highly suitable for screening the activity and researching the mechanisms of marine natural products.

For this Special Issue, we invite scientists from both academia and industry to submit articles highlighting the application of zebrafish models in the discovery of active marine natural products and the study of their mechanisms of action.

Dr. Xiaobin Li
Dr. Yun Zhang
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. Marine Drugs 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

  • marine drugs
  • zebrafish model
  • active natural product
  • bioactivity screening
  • mechanism of action
  • activity evaluation

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (3 papers)

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Research

13 pages, 8761 KiB  
Article
Protective Effect of Marine Peptide from Netunea arthritica cumingii Against Gentamicin-Induced Hair Cell Damage in Zebrafish
by Hongbao Zheng, Ranran Zhu, Yun Zhang, Kechun Liu, Qing Xia, Peihai Li, Xiaoyue Sun, Chen Sun and Shanshan Zhang
Mar. Drugs 2024, 22(11), 519; https://doi.org/10.3390/md22110519 - 16 Nov 2024
Viewed by 547
Abstract
Auditory hair cell damage induced by aminoglycoside antibiotics (AmAn) leads to hearing loss, which has a serious effect on people’s mental and physical health. This ototoxicity is thought to be related with the excessive accumulation of reactive oxygen species (ROS) in hair cells. [...] Read more.
Auditory hair cell damage induced by aminoglycoside antibiotics (AmAn) leads to hearing loss, which has a serious effect on people’s mental and physical health. This ototoxicity is thought to be related with the excessive accumulation of reactive oxygen species (ROS) in hair cells. However, therapeutic agents that protect hair cells are limited. Marine peptides have been shown to have excellent potential applications in disease prevention and treatment. Therefore, this study investigated the protective effects of an active peptide from Neptunea arthritica cumingii against AmAn-induced hair cell damage using the model of hair cell damage zebrafish. We identified the number, ultrastructure, and function of hair cells using fluorescence probes and scanning electron microscopy. The uptake of AmAn, ROS level, mitochondrial permeability transition pore, and apoptosis in hair cells were also tested by fluorescence labeling and TUNEL assay. The molecular mechanism for hair cell protection exerted by the peptide was detected by a real-time quantitative PCR assay. The results indicated that the peptide suppressed the uptake of AmAn but did not damage the function of hair cells mediating hearing. It also prevented ROS accumulation, decreased the occurrence of apoptosis, and rescued the abnormal opening and expressions of mitochondrial permeability transition pore and genes related to antioxidants. The peptide may be an effective therapeutic agent for AmAn-induced ototoxicity. In the future, we plan to use mammalian models to further investigate the otoprotective effect of the peptide. Full article
(This article belongs to the Special Issue Zebrafish Models in Marine Drug Discovery)
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19 pages, 99468 KiB  
Article
2-Acetamidophenol (2-AAP) Suppresses the Progression of Atherosclerosis by Alleviating Hyperlipidemia and Attenuating the Ferroptosis Pathway
by Xiaohan Zang, Yongcheng Wang, Cong Han, Lishuang Cui, Haojie Liu, Shuimiao Tian, Kechun Liu, Peihai Li, Chen Sun, Qing Xia and Yun Zhang
Mar. Drugs 2024, 22(11), 513; https://doi.org/10.3390/md22110513 - 13 Nov 2024
Viewed by 439
Abstract
Hyperlipidemia and consequent endothelial inflammation, along with foam cell generation, promote the progression of atherosclerosis (AS). Here, we aimed to investigate the effects of 2-acetamidophenol (2-AAP), which was selected by zebrafish phenotypic screening, in alleviating AS by relieving hyperlipidemia and inhibiting foam cell [...] Read more.
Hyperlipidemia and consequent endothelial inflammation, along with foam cell generation, promote the progression of atherosclerosis (AS). Here, we aimed to investigate the effects of 2-acetamidophenol (2-AAP), which was selected by zebrafish phenotypic screening, in alleviating AS by relieving hyperlipidemia and inhibiting foam cell formation, as well as the underlying mechanisms. In a zebrafish hyperlipidemia model, 2-AAP increased lipid-lowering efficacy; alleviated TC, TG, LDL-C, and MDA levels; elevated HDL-C and T-SOD levels; significantly improved intravascular macrophage aggregation; and improved blood flow. In an ox-LDL-induced RAW264.7 model, 2-AAP inhibited lipid phagocytosis in RAW264.7 cells; reduced the intracellular TC, TG, FC, and CE contents; and decreased the CE/TC ratio, thus slowing foam cell generation. In addition, 2-AAP alleviated intracellular ROS and ferrous ion accumulation in RAW264.7 cells, reduced the MDA content, and increased GPX4 viability. Furthermore, transcriptome analyses and gene expression validation showed 2-AAP treatment upregulates genes related to GSH synthesis and transport, such as gclc, gclm, gss, and gpx4a, and enhanced the expression levels of genes involved in the storage and transportation of iron ions, such as fpn1, fth, and g6pd, indicating that 2-AAP dramatically regulated the ferroptosis and glutathione metabolic pathways. Overall, our study demonstrated that 2-AAP demonstrated potential in AS by alleviating hyperlipidemia and attenuating the ferroptosis pathway and provided evidence supporting the future application of 2-AAP in AS treatment. Full article
(This article belongs to the Special Issue Zebrafish Models in Marine Drug Discovery)
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15 pages, 6260 KiB  
Article
Altechromone A Ameliorates Inflammatory Bowel Disease by Inhibiting NF-κB and NLRP3 Pathways
by Lei Li, Jing Huang, Lixin Feng, Liyan Xu, Houwen Lin, Kechun Liu, Xiaobin Li and Rongchun Wang
Mar. Drugs 2024, 22(9), 410; https://doi.org/10.3390/md22090410 - 9 Sep 2024
Viewed by 1055
Abstract
Altechromone A, also known as 2,5-dimethyl-7-hydroxychromone, is a hydroxyketone containing one hydroxyl and one ketone group. In this study, we isolated Altechromone A from the marine-derived fungus Penicillium Chrysogenum (XY-14-0-4). Previous reports show that Altechromone A has various activities including tumor suppression, antibacterial, [...] Read more.
Altechromone A, also known as 2,5-dimethyl-7-hydroxychromone, is a hydroxyketone containing one hydroxyl and one ketone group. In this study, we isolated Altechromone A from the marine-derived fungus Penicillium Chrysogenum (XY-14-0-4). Previous reports show that Altechromone A has various activities including tumor suppression, antibacterial, and antiviral activities. However, there is no study about its anti-inflammatory activity in inflammatory bowel disease (IBD). Here, we assess the anti-inflammatory activity, especially in IBD, and its potential mechanism using the zebrafish model. Our results indicated that Altechromone A has anti-inflammatory activity in a CuSO4-, tail-cutting-, and LPS-induced inflammatory model in zebrafish, respectively. In addition, Altechromone A greatly reduced the number of neutrophils, improved intestinal motility and efflux efficiency, alleviated intestinal damage, and reduced reactive oxygen species production in the TNBS-induced IBD zebrafish model. The transcriptomics sequencing and real-time qPCR indicated that Altechromone A inhibited the expression of pro-inflammatory genes including TNF-α, NF-κB, IL-1, IL-1β, IL-6, and NLRP3. Therefore, these data indicate that Altechromone A exhibits therapeutic effects in IBD by inhibiting the inflammatory response. Full article
(This article belongs to the Special Issue Zebrafish Models in Marine Drug Discovery)
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