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Inflammatory Tissue Response—How Nature Fights Back

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

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 1515

Special Issue Editors

Department of Biochemistry, Faculty of Medicine, University of Niš, 18 000 Niš, Serbia
Interests: inflammation; apoptosis; natural products; oxidative tissue damage; melatonin
Department of Physiology, Faculty of Medicine, University of Niš, 18000 Niš, Serbia
Interests: inflammatory cells; macrophages; cytokines; essential oils; nitric oxide

Special Issue Information

Dear Colleagues,

We live in an era where an uncontrolled utilization of drugs and the existence of drugs with numerous side effects deliver constant pressure on an ever-growing scientific population, demanding new drugs to target inflammatory responses. Nature-derived molecules have been a long-lasting inspiration of many а scientists when searching for such solutions. Since the discovery of acetylsalicylic acid from the bark of weeping willow, efforts focused on the discovery of nature-based molecules have increased. These research attempts have mainly found their rationale in the ethnomedicinal usage of some plants, and through a series of experiments, researchers have attempted to find an activity carrier. This Special Issue invites submissions focusing on the discovery of new natural products acting as anti-inflammatory agents or the rediscovery of known molecules with new anti-inflammatory activity, as well as comprehensive reviews.

This Special Issue is led by Dr. Dušan T. Sokolović and Dr. Nikola Stojanović (Department of Physiology, Faculty of Medicine, University of Niš, Niš, Serbia).

Dr. Dušan T. Sokolović
Dr. Nikola Stojanović
Guest Editors

Manuscript Submission Information

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Keywords

  • inflammatory response
  • immune response
  • naturally occurring molecules
  • cytokines

Published Papers (2 papers)

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Research

21 pages, 23976 KiB  
Article
Oregano (Origanum vulgare) Essential Oil and Its Constituents Prevent Rat Kidney Tissue Injury and Inflammation Induced by a High Dose of L-Arginine
Int. J. Mol. Sci. 2024, 25(2), 941; https://doi.org/10.3390/ijms25020941 - 11 Jan 2024
Viewed by 530
Abstract
This study aimed to evaluate the protective action of oregano (Origanum vulgare) essential oil and its monoterpene constituents (thymol and carvacrol) in L-arginine-induced kidney damage by studying inflammatory and tissue damage parameters. The determination of biochemical markers that reflect kidney function, [...] Read more.
This study aimed to evaluate the protective action of oregano (Origanum vulgare) essential oil and its monoterpene constituents (thymol and carvacrol) in L-arginine-induced kidney damage by studying inflammatory and tissue damage parameters. The determination of biochemical markers that reflect kidney function, i.e., serum levels of urea and creatinine, tissue levels of neutrophil-gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1), as well as a panel of oxidative-stress-related and inflammatory biomarkers, was performed. Furthermore, histopathological and immunohistochemical analyses of kidneys obtained from different experimental groups were conducted. Pre-treatment with the investigated compounds prevented an L-arginine-induced increase in serum and tissue kidney damage markers and, additionally, decreased the levels of inflammation-related parameters (TNF-α and nitric oxide concentrations and myeloperoxidase activity). Micromorphological kidney tissue changes correlate with the alterations observed in the biochemical parameters, as well as the expression of CD95 in tubule cells and CD68 in inflammatory infiltrate cells. The present results revealed that oregano essential oil, thymol, and carvacrol exert nephroprotective activity, which could be, to a great extent, associated with their anti-inflammatory, antiradical scavenging, and antiapoptotic action and, above all, due to their ability to lessen the disturbances arising from acute pancreatic damage. Further in-depth studies are needed in order to provide more detailed explanations of the observed activities. Full article
(This article belongs to the Special Issue Inflammatory Tissue Response—How Nature Fights Back)
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12 pages, 1576 KiB  
Article
Melatonin as a Promising Anti-Inflammatory Agent in an In Vivo Animal Model of Sepsis-Induced Rat Liver Damage
Int. J. Mol. Sci. 2024, 25(1), 455; https://doi.org/10.3390/ijms25010455 - 29 Dec 2023
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Abstract
Melatonin (MLT), earlier described as an effective anti-inflammatory agent, could be a beneficial adjunctive drug for sepsis treatment. This study aimed to determine the effects of MLT application in lipopolysaccharide (LPS)-induced sepsis in Wistar rats by determining the levels of liver tissue pro-inflammatory [...] Read more.
Melatonin (MLT), earlier described as an effective anti-inflammatory agent, could be a beneficial adjunctive drug for sepsis treatment. This study aimed to determine the effects of MLT application in lipopolysaccharide (LPS)-induced sepsis in Wistar rats by determining the levels of liver tissue pro-inflammatory cytokines (TNF-α, IL-6) and NF-κB as well as hematological parameters indicating the state of sepsis. Additionally, an immunohistological analysis of CD14 molecule expression was conducted. Our research demonstrated that treatment with MLT prevented an LPS-induced increase in pro-inflammatory cytokines TNF-α and IL-6 and NF-κB levels, and in the neutrophil to lymphocyte ratio (NLR). On the other hand, MLT prevented a decrease in the blood lymphocyte number induced by LPS administration. Also, treatment with MLT decreased the liver tissue expression of the CD14 molecule observed after sepsis induction. In summary, in rats with LPS-induced sepsis, MLT was shown to be a significant anti-inflammatory agent with the potential to change the liver’s immunological marker expression, thus ameliorating liver function. Full article
(This article belongs to the Special Issue Inflammatory Tissue Response—How Nature Fights Back)
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