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Processes
Special Issues
Pharmacodynamics Modeling of Anti-inflammatory Drugs
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Pharmacodynamics Modeling of Anti-inflammatory Drugs

A special issue of Processes (ISSN 2227-9717). This special issue belongs to the section "Pharmaceutical Processes".

Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 22188

Special Issue Editors

Prof. Dr. Wansu Park

E-Mail Website
Guest Editor
Department of Pathology, College of Korean Medicine, Gachon University, Seongnam-si 13120, Gyeonggi-do, Republic of Korea
Interests: inflammation; macrophage; cytokine; herbal medicine; nitric oxide; CHOP; ER stress; immunity; infection
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Myung Sook Oh

E-Mail Website
Guest Editor
College of Pharmacy, Kyung Hee University, Seoul 02447, Korea
Interests: neurotoxicity; neurodegenerative disorders; Parkinson’s disease; natural product
Prof. Dr. Jai-eun Kim

E-Mail Website
Guest Editor
College of Korean Medicine, Dongguk University, Goyang 10326, Republic of Korea
Interests: obesity; metabolic syndrome; inflammation; macrophage; natural product
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Immunity is an essential function for defending host against pathogenic infections. However, excessive immuno-inflammatory phenomena sometimes are resulted to be dangerous and harmful for life. For example, cytokine storm caused by viral infections might provoke the lung damage and acute respiratory distress syndrome. In addition, many reports have been suggested about inflammation-related carcinogenesis. Cancer-associated inflammation includes leukocyte infiltration, expression of cytokines (including chemokines and growth factors), tissue remodelling, and angiogenesis. In addition to cancer development, the unregulated inflammatory responses might contribute to chronic inflammatory diseases such as lupus, atherosclerosis, rheumatoid arthritis, osteoarthritis, psoriasis, vasculitis, chronic obstructive pulmonary disease, and irritable bowel disease. Thus, it is reasonable that biomedical researches needs to be performed for not only removal of invading pathogens but also regulation of immune and inflammatory responses. Recently, various natural products have been reported to have anti-inflammatory and analgesic effects. For clinical usages, more detailed investigation including on calcium signaling pathway in vitro or serum cytokine level in vivo deserves to be carried out.

This special issue on “Pharmacodynamics Modeling of Anti-Inflammatory Drugs” aims to establish a more detailed mechanism of action for natural product extract appropriate for precision medicine. Topics include, but are not limited to:

  • Development of new natural product extracts to modulate hyperproduction of cytokines in macrophages induced by pathogens;
  • Evaluation of anti-inflammatory effect of natural product extracts by suppressing the activation of STAT pathway;
  • Research on calcium signaling pathway in inflammation alleviated by natural product extracts
  • Study on effect of natural product extracts on inflammatory diseases related with mitogen-activated protein kinase;
  • Investigaton on analgesic and anti-inflammatory effect of natural product extracts with serum cytokine level.

Prof. Dr. Wansu Park
Prof. Dr. Myung Sook Oh
Prof. Dr. Jai-eun Kim
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. Processes 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 2400 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

  • Pharmacodynamics
  • Inflammation
  • Anti-Inflammation
  • Analgesic
  • Calcium
  • MAPK
  • STAT
  • Natural Product
  • Cytokine
  • Nitric Oxide
  • Immune Cell
  • Macrophage

Published Papers (5 papers)

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Editorial

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4 pages, 173 KiB  
Editorial
Special Issue on “Pharmacodynamics Modeling of Anti-Inflammatory Drugs”
by Jai-Eun Kim, Myung Sook Oh and Wansu Park
Processes 2023, 11(7), 2083; https://doi.org/10.3390/pr11072083 - 13 Jul 2023
Viewed by 726
Abstract
Immuno-inflammatory responses are essential for defending the host against pathogenic infections [...] Full article
(This article belongs to the Special Issue Pharmacodynamics Modeling of Anti-inflammatory Drugs)

Research

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23 pages, 4459 KiB  
Article
Mathematical Modeling of Eicosanoid Metabolism in Macrophage Cells: Cybernetic Framework Combined with Novel Information-Theoretic Approaches
by Lina Aboulmouna, Sana Khanum, Mohsen Heidari, Rubesh Raja, Shakti Gupta, Mano R. Maurya, Ananth Grama, Shankar Subramaniam and Doraiswami Ramkrishna
Processes 2023, 11(3), 874; https://doi.org/10.3390/pr11030874 - 15 Mar 2023
Cited by 1 | Viewed by 1776
Abstract
Cellular response to inflammatory stimuli leads to the production of eicosanoids—prostanoids (PRs) and leukotrienes (LTs)—and signaling molecules—cytokines and chemokines—by macrophages. Quantitative modeling of the inflammatory response is challenging owing to a lack of knowledge of the complex regulatory processes involved. Cybernetic models address [...] Read more.
Cellular response to inflammatory stimuli leads to the production of eicosanoids—prostanoids (PRs) and leukotrienes (LTs)—and signaling molecules—cytokines and chemokines—by macrophages. Quantitative modeling of the inflammatory response is challenging owing to a lack of knowledge of the complex regulatory processes involved. Cybernetic models address these challenges by utilizing a well-defined cybernetic goal and optimizing a coarse-grained model toward this goal. We developed a cybernetic model to study arachidonic acid (AA) metabolism, which included two branches, PRs and LTs. We utilized a priori biological knowledge to define the branch-specific cybernetic goals for PR and LT branches as the maximization of TNFα and CCL2, respectively. We estimated the model parameters by fitting data from three experimental conditions. With these parameters, we were able to capture a novel fourth independent experimental condition as part of the model validation. The cybernetic model enhanced our understanding of enzyme dynamics by predicting their profiles. The success of the model implies that the cell regulates the synthesis and activity of the associated enzymes, through cybernetic control variables, to accomplish the chosen biological goal. The results indicated that the dominant metabolites are PGD2 (a PR) and LTB4 (an LT), aligning with their corresponding known prominent biological roles during inflammation. Using heuristic arguments, we also infer that eicosanoid overproduction can lead to increased secretion of cytokines/chemokines. This novel model integrates mechanistic knowledge, known biological understanding of signaling pathways, and data-driven methods to study the dynamics of eicosanoid metabolism. Full article
(This article belongs to the Special Issue Pharmacodynamics Modeling of Anti-inflammatory Drugs)
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11 pages, 2562 KiB  
Article
Diospyrin Modulates Inflammation in Poly I:C-Induced Macrophages via ER Stress-Induced Calcium-CHOP Pathway
by Hyun-Ju Kim, Inamullah Khan, Adnan Shahidullah, Syed Muhammad Ashhad Halimi, Abdur Rauf, Ji-Young Lee, Young-Jin Kim, Bong-Youn Kim and Wansu Park
Processes 2020, 8(9), 1050; https://doi.org/10.3390/pr8091050 - 27 Aug 2020
Cited by 2 | Viewed by 2527
Abstract
Diospyrin, plant-derived bisnaphthoquinonoid, is known to have anticancer activity. However, pharmacological activity of diospyrin on viral infection is not well known. We investigated effects of diospyrin on macrophages induced by polyinosinic-polycytidylic acid (poly I:C), a mimic of double-stranded viral RNA. Various cytokines, intracellular [...] Read more.
Diospyrin, plant-derived bisnaphthoquinonoid, is known to have anticancer activity. However, pharmacological activity of diospyrin on viral infection is not well known. We investigated effects of diospyrin on macrophages induced by polyinosinic-polycytidylic acid (poly I:C), a mimic of double-stranded viral RNA. Various cytokines, intracellular calcium, nitric oxide (NO), phosphorylated p38 MAPK, and phosphorylated ERK1/2 as well as mRNA expressions of transcription factors were evaluated. Diospyrin significantly reduced NO production, granulocyte-macrophage colony-stimulating factor production, and intracellular calcium release in poly I:C-induced RAW 264.7. The phosphorylation of p38 MAPK and ERK1/2 was also significantly suppressed. Additionally, diospyrin inhibited mRNA levels of nitric oxide synthase 2, C/EBP homologous protein (CHOP), calcium/calmodulin dependent protein kinase II alpha, signal transducers and activators of transcription 1 (STAT1), STAT3, STAT4, Janus kinase 2, first apoptosis signal receptor, c-Jun, and c-Fos in poly I:C-induced RAW 264.7. Taken together, this study represents that diospyrin might have the inhibitory activity against viral inflammation such as excessive production of inflammatory mediators in poly I:C-induced RAW 264.7 via ER stress-induced calcium-CHOP pathway. Full article
(This article belongs to the Special Issue Pharmacodynamics Modeling of Anti-inflammatory Drugs)
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17 pages, 3225 KiB  
Article
Andrographis paniculata Extract Relieves Pain and Inflammation in Monosodium Iodoacetate-Induced Osteoarthritis and Acetic Acid-Induced Writhing in Animal Models
by Donghun Lee, Chae Yun Baek, Ji Hong Hwang and Mi-Yeon Kim
Processes 2020, 8(7), 873; https://doi.org/10.3390/pr8070873 - 20 Jul 2020
Cited by 7 | Viewed by 5022
Abstract
Osteoarthritis (OA), being the most prominent degenerative joint disease is affecting millions of elderly people worldwide. Although Andrographis paniculata is an ethnic medicine with a long history of being used as analgesic agent, no study using a monosodium iodoacetate (MIA) model has investigated [...] Read more.
Osteoarthritis (OA), being the most prominent degenerative joint disease is affecting millions of elderly people worldwide. Although Andrographis paniculata is an ethnic medicine with a long history of being used as analgesic agent, no study using a monosodium iodoacetate (MIA) model has investigated its potential activities against OA. In this study, experimental OA was induced in rats with a knee injection of MIA, which represents the pathological characteristics of OA in humans. A. paniculata extract (APE) substantially reversed the loss of hind limb weight-bearing and the cartilage damage resulted from the OA induction in rats. Additionally, the levels of serum pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α as well as the concentration of matrix metalloproteinases, including MMP-1, MMP-3, MMP-8, and MMP-13 were decreased by APE administration. Acetic acid-induced writhing responses in mice which quantitatively measure pain were significantly reduced by APE. In vitro, APE inhibited the generation of NO and downregulated the expression of IL-1β, IL-6, COX-2, and iNOS in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. The above results suggest the potential use APE as a therapeutic agent against OA. Full article
(This article belongs to the Special Issue Pharmacodynamics Modeling of Anti-inflammatory Drugs)
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Review

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16 pages, 250 KiB  
Review
Conflicting Effects of Coffee Consumption on Cardiovascular Diseases: Does Coffee Consumption Aggravate Pre-existing Risk Factors?
by Dongwoo Lim, Jiung Chang, Jungyun Ahn and Jaieun Kim
Processes 2020, 8(4), 438; https://doi.org/10.3390/pr8040438 - 8 Apr 2020
Cited by 15 | Viewed by 15900
Abstract
Coffee is one of the most popular beverages worldwide. Its effect on health is generally regarded as beneficial in many studies. However, there are growing concerns about the adverse effect of coffee consumption on cardiovascular disease (CVD) due to the potential aggravating impact [...] Read more.
Coffee is one of the most popular beverages worldwide. Its effect on health is generally regarded as beneficial in many studies. However, there are growing concerns about the adverse effect of coffee consumption on cardiovascular disease (CVD) due to the potential aggravating impact on the cardiovascular system attributed to various compounds within coffee. This review is focused on deteriorative effects of coffee consumption on CVDs with possible mechanisms. Patients with risk factors of CVDs should prudently consider heavy consumption of coffee as it may exacerbate hypertension, dyslipidemia, and atherosclerosis, and increase the odds of cardiovascular events. J-shaped or U-shaped dose-response graphs of coffee consumption and CVD parameters partially explain the inconsistency of conclusions between coffee studies on CVD, highlighting a moderate intake of coffee. Moreover, there are discrepancies in results from clinical studies elucidating considerable influences of confounding factors including gender and smoking status on outcomes of those conducted to reveal the actual impact of coffee consumption on CVDs. Physical features of subjects including genetic variations and body mass index (BMI) make it difficult to determine moderate intake of coffee for individuals in terms of caffeine metabolism. Further epidemiological studies with consideration about characteristics of the study population are needed to determine the exact effect of coffee consumption on CVD. Full article
(This article belongs to the Special Issue Pharmacodynamics Modeling of Anti-inflammatory Drugs)
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