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Marine Drugs
Special Issues
Pre-clinical Marine Drug Discovery Ⅱ
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Pre-clinical Marine Drug Discovery Ⅱ

A special issue of Marine Drugs (ISSN 1660-3397).

Deadline for manuscript submissions: closed (31 October 2022) | Viewed by 25071

Special Issue Editor

Prof. Dr. Jun Lu

grade E-Mail Website
Guest Editor
Auckland Bioengineering Institute, University of Auckland, Auckland 1142, New Zealand
Interests: diabetes; obesity; cancer; non-communicalbe diseases; marine natural compounds; fucoidan; seaweed; clams; food chemistry; pharmacology; drug metabolism; pharmacokinetics; pre-clinical pharmacology; natural compound extraction; polyamine metabolism; marine bioactives
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

After having had a successful Special Issue on the topic of “Pre-Clinical Marine Drug Discovery” about a year ago (see https://www.mdpi.com/journal/marinedrugs/special_issues/Pre_Clinical), I would like to call for a 2nd Special Issue on the same topic to continue to attract and present research output in this popular area.

Marine products provide ample opportunities for us to find bioactive compounds. To identify and confirm their bioactivities, pre-clinical studies are necessary before they can be developed further, either as health products or ultimately as medicine. There are plenty of pre-clinical tools and models for marine drug discovery. Through pre-clinical screening, many marine compounds have demonstrated important biological properties in the prevention and treatment of various diseases, including cancer, neurodegenerative diseases, obesity, diabetes, etc. Pre-clinical screening is a crucial step for discovering new lead compounds from marine products. This 2nd Special Issue on “Pre-Clinical Marine Drugs Discovery” will continue to gather the most relevant and new development research articles in the field since the closure of our previous Special Issue. We hope to capture the continuous progress and development in this important field. The issue is also a chance for scientists who are working on pre-clinical marine drug discovery to showcase their recent findings and attract the attention of marine drug developers.

Prof. Dr. Jun Lu
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. 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 products
  • Natural compounds
  • Pre-clinical screening
  • Mechanism of action
  • Extraction and analysis
  • Bioactive extracts and fractions
  • Pre-clinical models
  • Pre-clinical pharmacology
  • Molecular target

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Published Papers (6 papers)

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Research

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17 pages, 3069 KiB  
Article
A Paternal Fish Oil Diet Preconception Modulates the Gut Microbiome and Attenuates Necrotizing Enterocolitis in Neonatal Mice
by Jelonia T. Rumph, Victoria R. Stephens, Sharareh Ameli, Philip N. Gaines, Kevin G. Osteen, Kaylon L. Bruner-Tran and Pius N. Nde
Mar. Drugs 2022, 20(6), 390; https://doi.org/10.3390/md20060390 - 13 Jun 2022
Cited by 3 | Viewed by 3170
Abstract
Epidemiology and animal studies suggest that a paternal history of toxicant exposure contributes to the developmental origins of health and disease. Using a mouse model, our laboratory previously reported that a paternal history of in utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased his offspring’s [...] Read more.
Epidemiology and animal studies suggest that a paternal history of toxicant exposure contributes to the developmental origins of health and disease. Using a mouse model, our laboratory previously reported that a paternal history of in utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased his offspring’s risk of developing necrotizing enterocolitis (NEC). Additionally, our group and others have found that formula supplementation also increases the risk of NEC in both humans and mice. Our murine studies revealed that intervening with a paternal fish oil diet preconception eliminated the TCDD-associated outcomes that are risk factors for NEC (e.g., intrauterine growth restriction, delayed postnatal growth, and preterm birth). However, the efficacy of a paternal fish oil diet in eliminating the risk of disease development in his offspring was not investigated. Herein, reproductive-age male mice exposed to TCDD in utero were weaned to a standard or fish oil diet for one full cycle of spermatogenesis, then mated to age-matched unexposed females. Their offspring were randomized to a strict maternal milk diet or a supplemental formula diet from postnatal days 7–10. Offspring colon contents and intestines were collected to determine the onset of gut dysbiosis and NEC. We found that a paternal fish oil diet preconception reduced his offspring’s risk of toxicant-driven NEC, which was associated with a decrease in the relative abundance of the Firmicutes phylum, but an increase in the relative abundance of the Negativicutes class. Full article
(This article belongs to the Special Issue Pre-clinical Marine Drug Discovery Ⅱ)
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22 pages, 5004 KiB  
Article
The Endo-α(1,3)-Fucoidanase Mef2 Releases Uniquely Branched Oligosaccharides from Saccharina latissima Fucoidans
by Vy Ha Nguyen Tran, Thuan Thi Nguyen, Sebastian Meier, Jesper Holck, Hang Thi Thuy Cao, Tran Thi Thanh Van, Anne S. Meyer and Maria Dalgaard Mikkelsen
Mar. Drugs 2022, 20(5), 305; https://doi.org/10.3390/md20050305 - 29 Apr 2022
Cited by 20 | Viewed by 3581
Abstract
Fucoidans are complex bioactive sulfated fucosyl-polysaccharides primarily found in brown macroalgae. Endo-fucoidanases catalyze the specific hydrolysis of α-L-fucosyl linkages in fucoidans and can be utilized to tailor-make fucoidan oligosaccharides and elucidate new structural details of fucoidans. In this study, an endo-α(1,3)-fucoidanase encoding gene, [...] Read more.
Fucoidans are complex bioactive sulfated fucosyl-polysaccharides primarily found in brown macroalgae. Endo-fucoidanases catalyze the specific hydrolysis of α-L-fucosyl linkages in fucoidans and can be utilized to tailor-make fucoidan oligosaccharides and elucidate new structural details of fucoidans. In this study, an endo-α(1,3)-fucoidanase encoding gene, Mef2, from the marine bacterium Muricauda eckloniae, was cloned, and the Mef2 protein was functionally characterized. Based on the primary sequence, Mef2 was suggested to belong to the glycosyl hydrolase family 107 (GH107) in the Carbohydrate Active enZyme database (CAZy). The Mef2 fucoidanase showed maximal activity at pH 8 and 35 °C, although it could tolerate temperatures up to 50 °C. Ca2+ was shown to increase the melting temperature from 38 to 44 °C and was furthermore required for optimal activity of Mef2. The substrate specificity of Mef2 was investigated, and Fourier transform infrared spectroscopy (FTIR) was used to determine the enzymatic activity (Units per μM enzyme: Uf/μM) of Mef2 on two structurally different fucoidans, showing an activity of 1.2 × 10−3 Uf/μM and 3.6 × 10−3 Uf/μM on fucoidans from Fucus evanescens and Saccharina latissima, respectively. Interestingly, Mef2 was identified as the first described fucoidanase active on fucoidans from S. latissima. The fucoidan oligosaccharides released by Mef2 consisted of a backbone of α(1,3)-linked fucosyl residues with unique and novel α(1,4)-linked fucosyl branches, not previously identified in fucoidans from S. latissima. Full article
(This article belongs to the Special Issue Pre-clinical Marine Drug Discovery Ⅱ)
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15 pages, 3111 KiB  
Article
ω-3 DPA Protected Neurons from Neuroinflammation by Balancing Microglia M1/M2 Polarizations through Inhibiting NF-κB/MAPK p38 Signaling and Activating Neuron-BDNF-PI3K/AKT Pathways
by Baiping Liu, Yongping Zhang, Zhiyou Yang, Meijun Liu, Cai Zhang, Yuntao Zhao and Cai Song
Mar. Drugs 2021, 19(11), 587; https://doi.org/10.3390/md19110587 - 20 Oct 2021
Cited by 65 | Viewed by 5446
Abstract
Microglia M1 phenotype causes HPA axis hyperactivity, neurotransmitter dysfunction, and production of proinflammatory mediators and oxidants, which may contribute to the etiology of depression and neurodegenerative diseases. Eicosapentaenoic acid (EPA) may counteract neuroinflammation by increasing n-3 docosapentaenoic acid (DPA). However, the cellular and [...] Read more.
Microglia M1 phenotype causes HPA axis hyperactivity, neurotransmitter dysfunction, and production of proinflammatory mediators and oxidants, which may contribute to the etiology of depression and neurodegenerative diseases. Eicosapentaenoic acid (EPA) may counteract neuroinflammation by increasing n-3 docosapentaenoic acid (DPA). However, the cellular and molecular mechanisms of DPA, as well as whether it can exert antineuroinflammatory and neuroprotective effects, are unknown. The present study first evaluated DPA’s antineuroinflammatory effects in lipopolysaccharide (LPS)-activated BV2 microglia. The results showed that 50 μM DPA significantly decreased BV2 cell viability after 100 ng/mL LPS stimulation, which was associated with significant downregulation of microglia M1 phenotype markers and proinflammatory cytokines but upregulation of M2 markers and anti-inflammatory cytokine. Then, DPA inhibited the activation of mitogen-activated protein kinase (MAPK) p38 and nuclear factor-κB (NF-κB) p65 pathways, which results were similar to the effects of NF-κB inhibitor, a positive control. Second, BV2 cell supernatant was cultured with differentiated SH-SY5Y neurons. The results showed that the supernatant from LPS-activated BV2 cells significantly decreased SH-SY5Y cell viability and brain-derived neurotrophic factor (BDNF), TrkB, p-AKT, and PI3K expression, which were significantly reversed by DPA pretreatment. Furthermore, DPA neuroprotection was abrogated by BDNF-SiRNA. Therefore, n-3 DPA may protect neurons from neuroinflammation-induced damage by balancing microglia M1 and M2 polarizations, inhibiting microglia-NF-κB and MAPK p38 while activating neuron-BDNF/TrkB-PI3K/AKT pathways. Full article
(This article belongs to the Special Issue Pre-clinical Marine Drug Discovery Ⅱ)
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14 pages, 1725 KiB  
Article
Trikoramides B–D, Bioactive Cyanobactins from the Marine Cyanobacterium Symploca hydnoides
by Ma Yadanar Phyo, Teo Min Ben Goh, Jun Xian Goh and Lik Tong Tan
Mar. Drugs 2021, 19(10), 548; https://doi.org/10.3390/md19100548 - 28 Sep 2021
Cited by 10 | Viewed by 2547
Abstract
Three new cyanobactins, trikoramides B (1)–D (3), have been isolated from the marine cyanobacterium, Symploca hydnoides, following a preliminary bioassay-guided isolation of the two most active polar fractions based on the brine shrimp toxicity assay. These new cyanobactins [...] Read more.
Three new cyanobactins, trikoramides B (1)–D (3), have been isolated from the marine cyanobacterium, Symploca hydnoides, following a preliminary bioassay-guided isolation of the two most active polar fractions based on the brine shrimp toxicity assay. These new cyanobactins are new analogues of the previously reported cytotoxic trikoramide A (4) with differences mainly in the C-prenylated cyclotryptophan unit. Their planar structures were elucidated from their 1D and 2D NMR spectral data in combination with the HRMS/MS data. Marfey’s method, 2D NOESY NMR spectroscopic and ECD spectra analyses were used to determine the absolute stereochemistry of trikoramides B (1)–D (3). Trikoramides B (1) and D (3) exhibited cytotoxicity against MOLT-4 acute lymphoblastic leukemia cell line with IC50 values of 5.2 µM and 4.7 µM, respectively. Compounds 1 and 3 were also evaluated for their quorum-sensing inhibitory assay based on the Pseudomonas aeruginosa PAO1 lasB-gfp and rhlA-gfp bioreporter strains. Although trikoramide B (1) exhibited weak quorum-sensing inhibitory activity, the Br-containing trikoramide D (3) exhibited moderate to significant dose-dependent quorum-sensing inhibitory activities against PAO1 lasB-gpf and rhlA-gfp bioreporter strains with IC50 values of 19.6 µM and 7.3 µM, respectively. Full article
(This article belongs to the Special Issue Pre-clinical Marine Drug Discovery Ⅱ)
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15 pages, 16268 KiB  
Article
Dieckol Decreases Caloric Intake and Attenuates Nonalcoholic Fatty Liver Disease and Hepatic Lymphatic Vessel Dysfunction in High-Fat-Diet-Fed Mice
by Kyung-A Byun, Seyeon Oh, Myeongjoo Son, Chul-Hyun Park, Kuk Hui Son and Kyunghee Byun
Mar. Drugs 2021, 19(9), 495; https://doi.org/10.3390/md19090495 - 30 Aug 2021
Cited by 7 | Viewed by 2820
Abstract
Increased inflammation is the main pathophysiology of nonalcoholic fatty liver disease (NAFLD). Inflammation affects lymphatic vessel function that contributes to the removal of immune cells or macromolecules. Dysfunctional lymphatic vessels with decreased permeability are present in NAFLD. High-fat diet (HFD) is known to [...] Read more.
Increased inflammation is the main pathophysiology of nonalcoholic fatty liver disease (NAFLD). Inflammation affects lymphatic vessel function that contributes to the removal of immune cells or macromolecules. Dysfunctional lymphatic vessels with decreased permeability are present in NAFLD. High-fat diet (HFD) is known to increase body weight, food intake, and inflammation in the liver. Previously, it was reported that Ecklonia cava extracts (ECE) decreased food intake or weight gain, and low-calorie diet and weight loss is known as a treatment for NAFLD. In this study, the effects of ECE and dieckol (DK)—which is one component of ECE that decreases inflammation and increases lymphangiogenesis and lymphatic drainage by controlling lymphatic permeability in high-fat diet (HFD)-fed mice—on weight gain and food intake were investigated. ECE and DK decreased weight gain and food intake in the HFD-fed mice. NAFLD activities such as steatosis, lobular inflammation, and ballooning were increased by HFD and attenuated by ECE and DK. The expression of inflammatory cytokines such as IL-6 and TNF-α and infiltration of M1 macrophages were increased by HFD, and they were decreased by ECE or DK. The signaling pathways of lymphangiogenesis, VEGFR-3, PI3K/pAKT, and pERK were decreased by HFD, and they were restored by either ECE or DK. The expression of VE-cadherin (which represents lymphatic junctional function) was increased by HFD, although it was restored by either ECE or DK. In conclusion, ECE and DK attenuated NAFLD by decreasing weight gain and food intake, decreasing inflammation, and increasing lymphangiogenesis, as well as modulating lymphatic vessel permeability. Full article
(This article belongs to the Special Issue Pre-clinical Marine Drug Discovery Ⅱ)
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Review

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15 pages, 747 KiB  
Review
Potential Food and Nutraceutical Applications of Alginate: A Review
by Decheng Bi, Xu Yang, Lijun Yao, Zhangli Hu, Hui Li, Xu Xu and Jun Lu
Mar. Drugs 2022, 20(9), 564; https://doi.org/10.3390/md20090564 - 4 Sep 2022
Cited by 53 | Viewed by 6275
Abstract
Alginate is an acidic polysaccharide mainly extracted from kelp or sargassum, which comprises 40% of the dry weight of algae. It is a linear polymer consisting of β-D-mannuronic acid (M) and α-L-guluronic acid (G) with 1,4-glycosidic linkages, possessing various applications in the food [...] Read more.
Alginate is an acidic polysaccharide mainly extracted from kelp or sargassum, which comprises 40% of the dry weight of algae. It is a linear polymer consisting of β-D-mannuronic acid (M) and α-L-guluronic acid (G) with 1,4-glycosidic linkages, possessing various applications in the food and nutraceutical industries due to its unique physicochemical properties and health benefits. Additionally, alginate is able to form a gel matrix in the presence of Ca2+ ions. Alginate properties also affect its gelation, including its structure and experimental conditions such as pH, temperature, crosslinker concentration, residence time and ionic strength. These features of this polysaccharide have been widely used in the food industry, including in food gels, controlled-release systems and film packaging. This review comprehensively covers the analysis of alginate and discussed the potential applications of alginate in the food industry and nutraceuticals. Full article
(This article belongs to the Special Issue Pre-clinical Marine Drug Discovery Ⅱ)
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