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Natural Products: Potential New Anti-Inflammatory Drugs

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

Deadline for manuscript submissions: closed (31 December 2024) | Viewed by 2083

Special Issue Editor


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Guest Editor
1. Department of Pharmacology, School of Korean Medicine, Wonkwang University, Iksan 54538, Republic of Korea 2. Research Center of Traditional Korean Medicine, Wonkwang University, Iksan 54538, Republic of Korea
Interests: inflammation; pancreatitis; immunology; liver injury
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Special Issue Information

Dear Colleagues,

Inflammation is a biological process against harmful stimuli, such as outer pathogens, or injured cells, and is a prompt response to protect our body using immune cells and molecular mediators such as cytokines, and chemokines. Inflammation can be classified as either acute or chronic. When the harmful stimuli invade the human body, acute inflammation is initiated by the migration of leukocytes from the blood into the injured tissues. Biochemical inflammatory events operate locally, and the systemic body dysfunction of the vascular and immune system occurs. Prolonged inflammation, known as chronic inflammation, is characterized by the simultaneous destruction and healing of the tissue from the inflammatory process. Recently, there has been a discovery using Natural Medicine to regulate inflammatory reactions via cellular and molecular mechanisms. The dysfunction or hyper-stimulation of inflammation can lead to disorders underlying a vast variety of human diseases such as sepsis, cancer, atherosclerosis, pancreatitis, liver injury, and kidney injury. Exploring the anti-inflammatory properties of Natural Medicine provides a new therapy to combat these disorders.

This Research Topic aims to discover and develop novel natural compounds, single compounds, validated extracts, natural products, or combination formulas associated with Natural Medicines with anti-inflammatory properties in various experimental models. Topics of interest also include pharmacokinetics, metabolism, pharmacology, and toxicology related to the use of Natural Medicines. While Experimental Pharmacology and Drug Discovery is primarily centered on pharmacological research of new agents, novel pharmacodynamic and pharmacokinetic mechanisms that may explain or predict the clinical effects of Natural Medicines already in use and/or provide potential targets for drug development may also be welcome.

In this Research Topic, we welcome natural product-focused Original Research, Reviews, Clinical Trials, Methods, and Opinion articles that relate to but are not limited to the following aspects:

  • Novel natural compounds, single compounds, validated extracts, natural products, or combination formulas associated with Natural Medicines with anti-inflammatory properties.
  • Antioxidant/inflammatory activity of Natural Medicines in various experimental models.
  • Underlying novel mechanisms or pathways of Natural Medicines for the prevention and treatment of inflammatory diseases (in vitro and in vivo).
  • Clinical applications of Natural Medicines to treat inflammatory diseases.
  • The molecular mechanisms of inflammatory disease development.
  • Immuno-stimulation activity of Natural Medicines.

Dr. Gi-Sang Bae
Guest Editor

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Keywords

  • natural medicines
  • inflammatory diseases
  • anti-oxidation
  • anti-inflammatory mechanisms
  • cytokines

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Published Papers (2 papers)

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Research

21 pages, 11189 KiB  
Article
Novel Compounds Target Aberrant Calcium Signaling in the Treatment of Relapsed High-Risk Neuroblastoma
by Dana-Lynn T. Koomoa, Nathan Sunada, Italo Espinoza-Fuenzalida, Dustin Tacdol, Madeleine Shackleford, Li Feng, Dianqing Sun and Ingo Lange
Int. J. Mol. Sci. 2025, 26(7), 3180; https://doi.org/10.3390/ijms26073180 - 29 Mar 2025
Viewed by 377
Abstract
High-risk neuroblastoma (HRNB) is an extracranial solid pediatric cancer. Despite the plethora of treatments available for HRNB, up to 65% of patients are refractory or exhibit an initial response to treatment that transitions to therapy-resistant relapse, which is invariably fatal. A key feature [...] Read more.
High-risk neuroblastoma (HRNB) is an extracranial solid pediatric cancer. Despite the plethora of treatments available for HRNB, up to 65% of patients are refractory or exhibit an initial response to treatment that transitions to therapy-resistant relapse, which is invariably fatal. A key feature that promotes HRNB progression is aberrant calcium (Ca2+) signaling. Ca2+ signaling is regulated by several druggable channel proteins, offering tremendous therapeutic potential. Unfortunately, many of the Ca2+ channels in HRNB also perform fundamental functions in normal healthy cells, hence targeting them increases the potential for adverse effects. To overcome this challenge, we sought to identify novel Ca2+ signaling pathways that are observed in HRNB but not normal non-cancerous cells with the hypothesis that these novel pathways may serve as potential therapeutic targets. One Ca2+ signaling pathway that is deregulated in HRNB is store-operated Ca2+ entry (SOCE). SOCE relays the release of Ca2+ from the endoplasmic reticulum (ER) and Ca2+ influx via the plasma membrane and promotes cancer drug resistance by regulating transcriptional programming and the induction of mitochondrial Ca2+ (mtCa2+)-dependent signaling. mtCa2+ signaling is critical for cellular metabolism, reactive oxygen production, cell cycle, and proliferation and has a key role in the regulation of cell death. Therefore, a dynamic interplay between ER, SOCE, and mitochondria tightly regulates cell survival and apoptosis. From a library of synthesized novel molecules, we identified two structurally related compounds that uniquely disrupt the dynamic interplay between SOCE, ER, and mitochondrial signaling pathways and induce cell death in HRNB. Our results revealed that compounds 248 and 249 activate distinct aberrant Ca2+ signals that are unique to relapsed HRNB and could be exploited to induce mtCa+ overload, a novel calcium influx current, and subsequent cell death. These findings establish a potential new pathway of calcium-mediated cell death; targeting this pathway could be critical for the treatment of refractory and relapsed HRNB. Full article
(This article belongs to the Special Issue Natural Products: Potential New Anti-Inflammatory Drugs)
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14 pages, 3035 KiB  
Article
Protective Effects of Crotonis Semen Extract against Sepsis through NF-κB Pathway Inhibition
by Yo Sep Hwang, Hyang Ran Yoon, Hyo-Min Park, Jun-Pil Jang, Jun Hong Park, Seong-Hoon Park, Jong Seok Lim, Hee Jun Cho and Hee Gu Lee
Int. J. Mol. Sci. 2024, 25(18), 10089; https://doi.org/10.3390/ijms251810089 - 19 Sep 2024
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Abstract
Sepsis is an inflammatory condition causing organ failure due to an uncontrolled immune response to infection and remains a significant challenge. Crotonis Semen has displayed various pharmacological effects, yet its potential in protecting against sepsis and the mechanisms involved remains largely unclear. Here, [...] Read more.
Sepsis is an inflammatory condition causing organ failure due to an uncontrolled immune response to infection and remains a significant challenge. Crotonis Semen has displayed various pharmacological effects, yet its potential in protecting against sepsis and the mechanisms involved remains largely unclear. Here, we explored the antiseptic properties of Crotons Semen extract (CSE) in both LPS-stimulated J774 macrophages and mice subjected to sepsis through Cecal ligation and Puncture (CLP) or LPS induction. We found that CSE enhanced survival rates in mouse models with acute sepsis induced by CLP operation and LPS injection. Administering CSE also reduced levels of enzymes indicating organ damage, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatine kinase (CK), in septic mice. Furthermore, CSE lowered the serum levels of inflammatory mediators and cytokines, such as NO, TNF-α, IL-1β, and IL-6, in septic mice. In LPS-stimulated J774 macrophages, CSE reduced the expression of pro-inflammatory proteins, including iNOS and COX-2. Moreover, CSE inhibited the phosphorylation of IκBα and IKK, key components of the NF-κB signaling pathway, thereby reducing inflammatory mediators and cytokines. These results demonstrate CSE’s protective effects against sepsis through NF-κB pathway disruption, indicating its potential as a therapeutic option for acute inflammatory conditions. Full article
(This article belongs to the Special Issue Natural Products: Potential New Anti-Inflammatory Drugs)
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