Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Novel Anti-inflammatory Molecules

Special Issue Editors
Special Issue Information
Keywords
Related Special Issue
Published Papers

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

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 19410

Share This Special Issue

Special Issue Editor

Prof. Dr. Yuh-Lin Wu

E-Mail Website
Guest Editor

Department of Physiology, School of Medicine, National Yang-Ming University, No. 155, Sec. 2, Linong Street, Beitou District, Taipei 112, Taiwan
Interests: inflammation; cancer; ovary; ghrelin; interleukin-8; cyclooxygenase-2; granulosa cell; growth hormone releasing peptide-2
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammation is an essential part of the host defence system in response to internal and external stimuli, such infection or injury. A fine-tuned acute inflammation consequence lasting only for a short period of time is responsible for innate immunity or humoral immunity to provide a therapeutic role in body. However, when an acute inflammation shifts to a chronic type lasting for a long period of time, it may mediate a persistent production of inﬂammatory cytokines or other inflammatory mediators to result in pathogenesis of various inflammation-related diseases, including cancers. Thus, to identify a novel molecule performing high efficacy of anti-inflammatory function, but low side-effect or toxicity to cells or host should benefit a lot to human health. This Special Issue, “Novel Anti-inflammatory Molecules”, of the International Journal of Molecular Sciences aims to comprise a collection of research or review articles covering reports of any not-yet-sufficiently explored molecules possessing anti-inﬂammatory activities by using in vivo or vitro models to address the associated acting molecular signaling pathways are all welcome. The submitted manuscripts are expected to focus on any aspects in cellular, molecular, biochemical, or physiological mechanisms to reveal functional significance of such candidate anti-inflammation molecules.

Prof. Dr. Yuh-Lin Wu
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

inflammation
anti-inﬂammation
inﬂammatory disease
inﬂammatory mediators
cytokines
signal transduction

Related Special Issue

Novel Functions for Small Molecules in International Journal of Molecular Sciences (3 articles)

Published Papers (6 papers)

Download All Papers

Research

Jump to: Review

21 pages, 12037 KiB

Open AccessArticle

Amelioration of Endotoxin-Induced Acute Lung Injury and Alveolar Epithelial Cells Apoptosis by Simvastatin Is Associated with Up-Regulation of Survivin/NF-kB/p65 Pathway

by Lana Nežić, Ljiljana Amidžić, Ranko Škrbić, Radoslav Gajanin, Danijela Mandić, Jelena Dumanović, Zoran Milovanović and Vesna Jaćević

Int. J. Mol. Sci. 2022, 23(5), 2596; https://doi.org/10.3390/ijms23052596 - 26 Feb 2022

Cited by 11 | Viewed by 2624

Abstract

Disruption of the alveolar–endothelial barrier caused by inflammation leads to the progression of septic acute lung injury (ALI). In the present study, we investigated the beneficial effects of simvastatin on the endotoxin lipopolysaccharide (LPS)-induced ALI and its related mechanisms. A model of ALI was induced within experimental sepsis developed by intraperitoneal injection of a single non-lethal LPS dose after short-term simvastatin pretreatment (10–40 mg/kg orally). The severity of the lung tissue inflammatory injury was expressed as pulmonary damage scores (PDS). Alveolar epithelial cell apoptosis was confirmed by TUNEL assay (DNA fragmentation) and expressed as an apoptotic index (AI), and immunohistochemically for cleaved caspase-3, cytochrome C, and anti-apoptotic Bcl-xL, an inhibitor of apoptosis, survivin, and transcriptional factor, NF-kB/p65. Severe inflammatory injury of pulmonary parenchyma (PDS 3.33 ± 0.48) was developed after the LPS challenge, whereas simvastatin significantly and dose-dependently protected lung histology after LPS (p < 0.01). Simvastatin in a dose of 40 mg/kg showed the most significant effects in amelioration alveolar epithelial cells apoptosis, demonstrating this as a marked decrease of AI (p < 0.01 vs. LPS), cytochrome C, and cleaved caspase-3 expression. Furthermore, simvastatin significantly enhanced the expression of Bcl-xL and survivin. Finally, the expression of survivin and its regulator NF-kB/p65 in the alveolar epithelium was in strong positive correlation across the groups. Simvastatin could play a protective role against LPS-induced ALI and apoptosis of the alveolar–endothelial barrier. Taken together, these effects were seemingly mediated by inhibition of caspase 3 and cytochrome C, a finding that might be associated with the up-regulation of cell-survival survivin/NF-kB/p65 pathway and Bcl-xL. Full article

(This article belongs to the Special Issue Novel Anti-inflammatory Molecules)

► Show Figures

Figure 1

15 pages, 2173 KiB

Open AccessArticle

Anti-Septic Functions of Cornuside against HMGB1-Mediated Severe Inflammatory Responses

by Nayeon Kim, Chaeyeong Kim, Soo Ho Ryu, Wonhwa Lee and Jong-Sup Bae

Int. J. Mol. Sci. 2022, 23(4), 2065; https://doi.org/10.3390/ijms23042065 - 13 Feb 2022

Cited by 7 | Viewed by 2247

Abstract

High mobility group box 1 (HMGB1) is acknowledged to have critical functions; therefore, targeting this protein may have therapeutic effects. One example is potential antiseptic activity obtained by suppressing HMGB1 secretion, leading to the recovery of vascular barrier integrity. Cornuside (CN), which is a product extracted from the fruit of Cornusofficinalis Seib, is a natural bis-iridoid glycoside with the therapeutic effects of suppressing inflammation and regulating immune responses. However, the mechanism of action of CN and impact on sepsis is still unclear. We examined if CN could suppress HMGB1-induced excessive permeability and if the reduction of HMGB1 in response to LPS treatment increased the survival rate in a mouse model of sepsis. In human endothelial cells stimulated by LPS and mice with septic symptoms of cecal ligation and puncture (CLP), we examined levels of proinflammatory proteins and biomarkers as an index of tissue damage, along with decreased vascular permeability. In both LPS-treated human umbilical vein endothelial cells (HUVECs) and the CLP-treated mouse model of sepsis, we applied CN after the induction processes were over. CN suppressed excessive permeability and inhibited HMGB1 release, leading to the amelioration of vascular instability, reduced mortality, and improved histological conditions in the CLP-induced septic mouse model. Overall, we conclude that the suppressed release of HMGB1 and the increased survival rate of mice with CLP-induced sepsis caused by CN may be an effective pharmaceutical treatment for sepsis. Full article

(This article belongs to the Special Issue Novel Anti-inflammatory Molecules)

► Show Figures

Figure 1

Review

Jump to: Research

21 pages, 1373 KiB

Open AccessReview

Neurodegenerative Diseases: Can Caffeine Be a Powerful Ally to Weaken Neuroinflammation?

by Melania Ruggiero, Rosa Calvello, Chiara Porro, Giovanni Messina, Antonia Cianciulli and Maria Antonietta Panaro

Int. J. Mol. Sci. 2022, 23(21), 12958; https://doi.org/10.3390/ijms232112958 - 26 Oct 2022

Cited by 12 | Viewed by 6020

Abstract

In recent years, there has been considerable research showing that coffee consumption seems to be beneficial to human health, as it contains a mixture of different bioactive compounds such as chlorogenic acids, caffeic acid, alkaloids, diterpenes and polyphenols. Neurodegenerative diseases (NDs) are debilitating, and non-curable diseases associated with impaired central, peripheral and muscle nervous systems. Several studies demonstrate that neuroinflammation mediated by glial cells—such as microglia and astrocytes—is a critical factor contributing to neurodegeneration that causes the dysfunction of brain homeostasis, resulting in a progressive loss of structure, function, and number of neuronal cells. This happens over time and leads to brain damage and physical impairment. The most known chronic NDs are represented by Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD). According to epidemiological studies, regular coffee consumption is associated with a lower risk of neurodegenerative diseases. In this review, we summarize the latest research about the potential effects of caffeine in neurodegenerative disorders prevention and discuss the role of controlled caffeine delivery systems in maintaining high plasma caffeine concentrations for an extended time. Full article

(This article belongs to the Special Issue Novel Anti-inflammatory Molecules)

► Show Figures

Graphical abstract

13 pages, 1015 KiB

Open AccessReview

Targeting Persistent Neuroinflammation after Hypoxic-Ischemic Encephalopathy—Is Exendin-4 the Answer?

by Kelly Q. Zhou, Simerdeep K. Dhillon, Laura Bennet, Alistair J. Gunn and Joanne O. Davidson

Int. J. Mol. Sci. 2022, 23(17), 10191; https://doi.org/10.3390/ijms231710191 - 05 Sep 2022

Cited by 6 | Viewed by 2398

Abstract

Hypoxic-ischemic encephalopathy is brain injury resulting from the loss of oxygen and blood supply around the time of birth. It is associated with a high risk of death or disability. The only approved treatment is therapeutic hypothermia. Therapeutic hypothermia has consistently been shown to significantly reduce the risk of death and disability in infants with hypoxic-ischemic encephalopathy. However, approximately 29% of infants treated with therapeutic hypothermia still develop disability. Recent preclinical and clinical studies have shown that there is still persistent neuroinflammation even after treating with therapeutic hypothermia, which may contribute to the deficits seen in infants despite treatment. This suggests that potentially targeting this persistent neuroinflammation would have an additive benefit in addition to therapeutic hypothermia. A potential additive treatment is Exendin-4, which is a glucagon-like peptide 1 receptor agonist. Preclinical data from various in vitro and in vivo disease models have shown that Exendin-4 has anti-inflammatory, mitochondrial protective, anti-apoptotic, anti-oxidative and neurotrophic effects. Although preclinical studies of the effect of Exendin-4 in perinatal hypoxic-ischemic brain injury are limited, a seminal study in neonatal mice showed that Exendin-4 had promising neuroprotective effects. Further studies on Exendin-4 neuroprotection for perinatal hypoxic-ischemic brain injury, including in large animal translational models are warranted to better understand its safety, window of opportunity and effectiveness as an adjunct with therapeutic hypothermia. Full article

(This article belongs to the Special Issue Novel Anti-inflammatory Molecules)

► Show Figures

Figure 1

21 pages, 1783 KiB

Open AccessReview

Vitamin D–VDR Novel Anti-Inflammatory Molecules—New Insights into Their Effects on Liver Diseases

by Ioanna Aggeletopoulou, Konstantinos Thomopoulos, Athanasia Mouzaki and Christos Triantos

Int. J. Mol. Sci. 2022, 23(15), 8465; https://doi.org/10.3390/ijms23158465 - 30 Jul 2022

Cited by 8 | Viewed by 2495

Abstract

There is consistent evidence that vitamin D deficiency is strongly associated with liver dysfunction, disease severity, and poor prognosis in patients with liver disease. Vitamin D and its receptor (VDR) contribute to the regulation of innate and adaptive immune responses. The presence of genetic variants of vitamin D- and VDR-associated genes has been associated with liver disease progression. In our recent work, we summarized the progress in understanding the molecular mechanisms involved in vitamin D–VDR signaling and discussed the functional significance of VDR signaling in specific cell populations in liver disease. The current review focuses on the complex interaction between immune and liver cells in the maintenance of liver homeostasis and the development of liver injury, the interplay of vitamin D and VDR in the development and outcome of liver disease, the role of vitamin D- and VDR-associated genetic variants in modulating the occurrence and severity of liver disease, and the therapeutic value of vitamin D supplementation in various liver diseases. The association of the vitamin D–VDR complex with liver dysfunction shows great potential for clinical application and supports its use as a prognostic index and diagnostic tool. Full article

(This article belongs to the Special Issue Novel Anti-inflammatory Molecules)

► Show Figures

Figure 1

17 pages, 920 KiB

Open AccessReview

Emerging Roles of the Iron Chelators in Inflammation

by Alessandra Di Paola, Chiara Tortora, Maura Argenziano, Maria Maddalena Marrapodi and Francesca Rossi

Int. J. Mol. Sci. 2022, 23(14), 7977; https://doi.org/10.3390/ijms23147977 - 20 Jul 2022

Cited by 31 | Viewed by 2836

Abstract

Iron is a crucial element for mammalian cells, considering its intervention in several physiologic processes. Its homeostasis is finely regulated, and its alteration could be responsible for the onset of several disorders. Iron is closely related to inflammation; indeed, during inflammation high levels of interleukin-6 cause an increased production of hepcidin which induces a degradation of ferroportin. Ferroportin degradation leads to decreased iron efflux that culminates in elevated intracellular iron concentration and consequently iron toxicity in cells and tissues. Therefore, iron chelation could be considered a novel and useful therapeutic strategy in order to counteract the inflammation in several autoimmune and inflammatory diseases. Several iron chelators are already known to have anti-inflammatory effects, among them deferiprone, deferoxamine, deferasirox, and Dp44mT are noteworthy. Recently, eltrombopag has been reported to have an important role in reducing inflammation, acting both directly by chelating iron, and indirectly by modulating iron efflux. This review offers an overview of the possible novel biological effects of the iron chelators in inflammation, suggesting them as novel anti-inflammatory molecules. Full article

(This article belongs to the Special Issue Novel Anti-inflammatory Molecules)

► Show Figures

Figure 1

Journal Menu

Journal Browser

Novel Anti-inflammatory Molecules

Share This Special Issue

Special Issue Editor

Special Issue Information

Keywords

Related Special Issue

Published Papers (6 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI