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Bioactive Compounds: Potential New Anti-inflammatory Drugs 2.0

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 7419

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Prof. Dr. Yu-Hsiang Kuan

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Guest Editor

Department of Pharmacology, School of Medicine, Chung Shan Medical University, No. 110, Sec. 1, Jianguo N. Rd., Taichung 402, Taiwan
Interests: apoptosis; inflammation; genotoxicity; acute lung injury; cellular signal
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Prof. Dr. Chunjung Chen

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Guest Editor

Department of Medical Research, Taichung Veterans General Hospital, Taichung 407, Taiwan
Interests: luteolin; brain inflammation
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Special Issue Information

Dear Colleagues,

Inflammation is the important process of overexpression of proinflammatory and bactericidal mediators in the elimination of invasive pathogens and microbes. Acute and chronic inflammation leads to several diseases, such as acute lung injury, acute kidney injury, pneumonia, chronic obstructive pulmonary disease, hepatitis, cardiovascular disease, cancer, arthritis, spondylitis, etc. The World Health Organization (WHO) has proposed that inflammatory diseases are the greatest threat to human health in the world. The development of compounds able to effectively reduce inflammatory responses and have no adverse effects is a topic of popular concern. Bioactive compounds are molecules and found in natural products including animals, plants, microbes, marine organisms. Bioactive compounds appear to have health benefits and therapeutic effects via anti-inflammation, anti-oxidation, immunomodulation, and anti-toxic effect. A growing number of signal transductions participate in the regulation of inflammation, including the MAPK family pathway, the IkB/NFkB pathway, the JAK/STAT pathway, the priming and activating NLRP3 inflammasome, cytokine storm, the pyroptosis pathway, the apoptotic pathway, etc.

This Special Issue aims to cover original and review articles presenting outstanding data on the development of new bioactive compounds and relative molecular mechanisms for anti-inflammation.

Prof. Dr. Yu-Hsiang Kuan
Prof. Dr. Chunjung Chen
Guest Editors

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Keywords

bioactive compounds
anti-inflammation
anti-oxidation
immunomodulation
anti-toxic effect
health beneficial effect
signal transduction

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Published Papers (4 papers)

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Research

15 pages, 6291 KiB

Open AccessArticle

Anti-Proteolytic Peptide R7I Protects the Intestinal Barrier and Alleviates Fatty Acid Malabsorption in Salmonella typhimurium-Infected Mice

by Yunzhe Su, Taotao Sun, Junhan Gao, Chenxu Zhang, Xuesheng Liu, Chongpeng Bi, Jiajun Wang and Anshan Shan

Int. J. Mol. Sci. 2023, 24(22), 16409; https://doi.org/10.3390/ijms242216409 - 16 Nov 2023

Cited by 1 | Viewed by 1263

Abstract

With a wide range of hosts, environmental adaptation, and antibiotic resistance, Salmonella typhimurium is one of the most common causes of food poisoning in the world. Infection with Salmonella typhimurium not only results in intestinal inflammation but also damages the intestinal barrier and interferes with the host’s ability to absorb nutrients. It is imperative to find alternatives to antibiotics for eradicating bacteria, reducing intestinal damage, and reestablishing nutrient absorption, especially given that antibiotics are currently prohibited. This research aims to understand the protective role of anti-proteolytic peptide R7I on the gut in the setting of Salmonella typhimurium infection and its impact on nutritional absorption, maybe offering an alternative to antibiotics for bacterial killing. The findings demonstrated that R7I reduced the production of inflammatory factors, including IL-6, TNF-α, and L-1β in the jejunum and decreased the expression of genes like TLR4 and NF-κB in the jejunum (p < 0.05). R7I enhanced antioxidant capacity and preserved the antioxidant/pro-oxidant balance in the jejunum (p < 0.05). R7I also normalized intestinal shape and restored tight junction protein expression. Fatty acid binding protein 2 (FABP2) and fatty acid transport protein 4 (FATP4) expression in the jejunum was restored by R7I. In addition, serum-free fatty acids and lipid metabolites were significantly higher in the R7I group than in the control group (p < 0.05). Overall, the anti-enzyme peptide R7I maintained the healthy state of the intestine and alleviated the abnormal fatty acid absorption caused by bacterial infection. Full article

(This article belongs to the Special Issue Bioactive Compounds: Potential New Anti-inflammatory Drugs 2.0)

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15 pages, 3279 KiB

Open AccessArticle

CC5 and CC8, Two Disintegrin Isoforms from Cerastes cerastes Snake Venom Decreased Inflammation Response In Vitro and In Vivo

by Maram Morjen, Ons Zakraoui, Zaineb Abdelkafi-Koubaa, Najet Srairi-Abid, Naziha Marrakchi, Khadija Essafi-Benkhadir and Jed Jebali

Int. J. Mol. Sci. 2023, 24(15), 12427; https://doi.org/10.3390/ijms241512427 - 4 Aug 2023

Cited by 4 | Viewed by 1593

Abstract

Inflammation is associated with many pathology disorders and the malignant progression of most cancers. Therefore, targeting inflammatory pathways could provide a promising strategy for disease prevention and treatment. In this study, we experimentally investigated the anti-inflammatory effect of CC5 and CC8, two disintegrin isoforms isolated from Cerastes cerastes snake venom, on LPS-stimulated macrophages, both on human THP-1 and mouse RAW264.7 cell adherence and their underlying mechanisms by measuring cytokine release levels and Western blot assay. Equally, both molecules were evaluated on a carrageenan-induced edema rat model. Our findings suggest that CC5 and CC8 were able to reduce adhesion of LPS-stimulated macrophages both on human THP-1 and mouse RAW264.7 cells to fibrinogen and vitronectin through the interaction with the αvβ3 integrin receptor. Moreover, CC5 and CC8 reduced the levels of reactive oxygen species (ROS) mediated by the NF-κB, MAPK and AKT signaling pathways that lead to decreased production of the pro-inflammatory cytokines TNF-α, IL-6 and IL-8 and increased secretion of IL-10 in LPS-stimulated THP-1 and RAW264.7 cells. Interestingly, both molecules potently exhibited an anti-inflammatory effect in vivo by reducing paw swelling in rats. In light of these results, we can propose the CC5 and CC8 disintegrins as interesting tools to design potential candidates against inflammatory-related diseases. Full article

(This article belongs to the Special Issue Bioactive Compounds: Potential New Anti-inflammatory Drugs 2.0)

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15 pages, 3637 KiB

Open AccessArticle

Effect of Hesperidin on Barrier Function and Reactive Oxygen Species Production in an Oral Epithelial Cell Model, and on Secretion of Macrophage-Derived Inflammatory Mediators during Porphyromonas gingivalis Infection

by Patricia Milagros Maquera-Huacho, Denise Palomari Spolidorio, John Manthey and Daniel Grenier

Int. J. Mol. Sci. 2023, 24(12), 10389; https://doi.org/10.3390/ijms241210389 - 20 Jun 2023

Cited by 4 | Viewed by 2002

Abstract

Porphyromonas gingivalis is a periodontopathogenic bacterium that can adhere to and colonize periodontal tissues, leading to an inflammatory process, and, consequently, tissue destruction. New therapies using flavonoids, such as hesperidin, are being studied, and their promising properties have been highlighted. The aim of this study was to evaluate the effect of hesperidin on the epithelial barrier function, reactive oxygen species (ROS) production, and on the inflammatory response caused by P. gingivalis in in vitro models. The integrity of the epithelial tight junctions challenged by P. gingivalis was determined by monitoring the transepithelial electrical resistance (TER). P. gingivalis adherence to a gingival keratinocyte monolayer and a basement membrane model were evaluated by a fluorescence assay. A fluorometric assay was used to determine the ROS production in gingival keratinocytes. The level of pro-inflammatory cytokines and matrix metalloproteinases (MMPs) secretion was evaluated by ELISA; to assess NF-κB activation, the U937-3xjB-LUC monocyte cell line transfected with a luciferase reporter gene was used. Hesperidin protected against gingival epithelial barrier dysfunction caused by P. gingivalis and reduced the adherence of P. gingivalis to the basement membrane model. Hesperidin dose-dependently inhibited P. gingivalis-mediated ROS production by oral epithelial cells as well as the secretion of IL-1β, TNF-α, IL-8, MMP-2, and MMP-9 by macrophages challenged with P. gingivalis. Additionally, it was able to attenuate NF-κB activation in macrophages stimulated with P. gingivalis. These findings suggest that hesperidin has a protective effect on the epithelial barrier function, in addition to reducing ROS production and attenuating the inflammatory response associated with periodontal disease. Full article

(This article belongs to the Special Issue Bioactive Compounds: Potential New Anti-inflammatory Drugs 2.0)

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13 pages, 4157 KiB

Open AccessArticle

Chalcone T4 Inhibits RANKL-Induced Osteoclastogenesis and Stimulates Osteogenesis In Vitro

by Iolanda Augusta Fernandes de Matos, Natalie Aparecida Rodrigues Fernandes, Giovani Cirelli, Mariely Araújo de Godoi, Letícia Ribeiro de Assis, Luis Octávio Regasini, Carlos Rossa Junior and Morgana Rodrigues Guimarães-Stabili

Int. J. Mol. Sci. 2023, 24(8), 7624; https://doi.org/10.3390/ijms24087624 - 21 Apr 2023

Viewed by 1779

Abstract

Chalcones are phenolic compounds produced during the biosynthesis of flavonoids that have numerous biological activities, including anti-inflammatory, antioxidant and anticancer. In this in vitro study, we investigate a newly synthesized chalcone (Chalcone T4) in the context of bone turnover, specifically on the modulation of osteoclast differentiation and activity and osteoblast differentiation. Murine macrophages (RAW 264.7) and pre-osteoblasts (MC3T3-E1) were used as models of osteoclasts and osteoblasts, respectively. Differentiation and activity osteoclasts were induced by RANKL in the presence and absence of non-cytotoxic concentrations of Chalcone T4, added in different periods during osteoclastogenesis. Osteoclast differentiation and activity were assessed by actin ring formation and resorption pit assay, respectively. Expression of osteoclast-specific markers (Nfatc1, Oscar, Acp5, Mmp-9 and Ctsk) was determined by RT-qPCR, and the activation status of relevant intracellular signaling pathways (MAPK, AKT and NF-kB) by Western blot. Osteoblast differentiation and activity was induced by osteogenic culture medium in the presence and absence of the same concentrations of Chalcone T4. Outcomes assessed were the formation of mineralization nodules via alizarin red staining and the expression of osteoblast-related genes (Alp e Runx2) by RT-qPCR. Chalcone T4 reduced RANKL-induced osteoclast differentiation and activity, suppressed Oscar, Acp5 and Mmp-9 expression, and decreased ERK and AKT activation in a dose-dependent manner. Nfact1 expression and NF-kB phosphorylation were not modulated by the compound. Mineralized matrix formation and the expression of Alp and Runx2 by MC3T3-E1 cells were markedly stimulated by Chalcone T4. Collectively, these results demonstrate that Chalcone T4 inhibits in osteoclast differentiation and activity and stimulates osteogenesis, which indicates a promising therapeutic potential in osteolytic diseases. Full article

(This article belongs to the Special Issue Bioactive Compounds: Potential New Anti-inflammatory Drugs 2.0)

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