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Background: Mentha longifolia L. is a perennial plant belonging to the Lamiaceae family that has a wide distribution in the world. M. longifolia has many applications in the food and pharmaceutical industries due to its terpenoid and phenolic compounds. The phytochemical profile and biological activity of plants are affected by their genetics and habitat conditions. In the present study, the content, constituents and antifungal activity of the essential oil extracted from 20 accessions of M. longifolia collected from different regions of Iran and Iraq countries were evaluated., Results: The essential oil content of the accessions varied between 1.54 ± 0.09% (in the Divandarreh accession) to 5.49 ± 0.12% (in the Khabat accession). Twenty-seven compounds were identified in the essential oils of the studied accessions, which accounted for 85.5-99.61% of the essential oil. The type and amount of dominant compounds in the essential oil were different depending on the accession. Cluster analysis of accessions based on essential oil compounds grouped them into three clusters. The first cluster included Baziyan, Boukan, Sarouchavah, Taghtagh, Darbandikhan, Isiveh and Harir. The second cluster included Khabat, Kounamasi, Soni and Mahabad, and other accessions were included in the third cluster. Significant correlations were observed between the essential oil content and components with the climatic and soil conditions of the habitats. The M. longifolia essential oil indicated antifungal activity against Fusarium solani in both methods used. In all studied accessions, the fumigation method compared to the contact method was more able to control mycelia growth. In both methods, the inhibition percentage of essential oil on mycelia growth increased with an increase in essential oil concentration. Significant correlations were found between the essential oil components and the inhibition percentage of mycelium growth., Conclusion: The studied M. longifolia accessions showed significant differences in terms of the essential oil content and components. Differences in phytochemical profile of accessions can be due to their genetic or habitat conditions. The distance of the accessions in the cluster was not in accordance with their geographical distance, which indicates the more important role of genetic factors compared to habitat conditions in separating accessions. The antifungal activity of essential oils was strongly influenced by the essential oil quality and concentration, as well as the application method. Determining and introducing the elite accession in this study can be different depending on the breeder's aims, such as essential oil content, desired chemical composition, or antifungal activity., (© 2024. The Author(s).)

Objective: The aim of this study is to understand the role of cannabinoid type 2 receptor (CB2R) during periodontal inflammation and to identify anti-inflammatory agents for the development of drugs to treat periodontitis (PD)., Background: Cannabinoid type 2 receptor is found in periodontal tissue at sites of inflammation/infection. Our previous study demonstrated anti-inflammatory responses in human periodontal ligament fibroblasts (hPDLFs) via CB2R ligands., Methods: Anandamide (AEA), HU-308 (agonist), and SMM-189 (inverse agonist) were tested for effects on IL-1β-stimulated cytokines, chemokines, and angiogenic and vascular markers expressed by hPDLFs using Mesoscale Discovery V-Plex Kits. Signal transduction pathways (p-c-Jun, p-ERK, p-p-38, p-JNK, p-CREB, and p-NF-kB) were investigated using Cisbio HTRF kits. ACTOne and Tango™ -BLA functional assays were used to measure cyclic AMP (cAMP) and β-arrestin activity., Results: IL-1β stimulated hPDLF production of 18/39 analytes, which were downregulated by the CB2R agonist and the inverse agonist. AEA exhibited pro-inflammatory and anti-inflammatory effects. IL-1β increased phosphoproteins within the first hour except p-JNK. CB2R ligands attenuated p-p38 and p-NFĸB, but a late rise in p-38 was seen with HU-308. As p-ERK levels declined, a significant increase in p-ERK was observed later in the time course by synthetic CB2R ligands. P-JNK was significantly affected by SMM-189 only, while p-CREB was elevated significantly by CB2R ligands at 180 minutes. HU-308 affected both cAMP and β-arrestin pathway. SMM-189 only stimulated cAMP., Conclusion: The findings that CB2R agonist and inverse agonist may potentially regulate inflammation suggest that development of CB2R therapeutics could improve on current treatments for PD and other oral inflammatory pathologies., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Periodontitis is a chronic inflammatory disease in the oral cavity caused by bacterial biofilm attached to tooth surfaces. The periodontal pathogenic microorganisms trigger the disease process; however, the destruction of the periodontium is mostly caused by the host's immune response to the bacterial insults. The main thrust of periodontal therapy has been centered traditionally on reducing the microbial load by mechanical and antimicrobial means. This approach has been reported to be effective for the majority of patients and sites. However, modulating the host response by anti-inflammatory agents could provide another viable pathway to managing poorly responding periodontal patients. The overall objective of this paper is to review current data pertinent to curcumin and its dual anti-inflammatory and antimicrobial properties and to explore its potential in managing patients with periodontal diseases. Curcumin has a wide biological spectrum that could provide clinicians with an alternative anti-inflammatory and antimicrobial agent for managing a variety of maladies including periodontal diseases. However, large-scale longitudinal randomized clinical trials are needed to prove efficacy and effectiveness of curcumin in managing periodontitis. Furthermore, its structure requires modification in order to improve its bioavailability and its clinical effectiveness. Further research aiming at improving its delivery and formulation will enhance its dual potential as an important anti-inflammatory and anti-microbial agent in periodontology., (Copyright© by the International Academy of Periodontology.)

Two-dimensional isoelectric focusing and gel electrophoresis followed by mass spectrometry were used to detect, measure, and identify changes in protein expression correlated with differences in the metastatic potential of cultured rat mammary adenocarcinoma cells. MTC is a non-metastatic cell clone derived from a primary tumor. MTLn2 and MTLn3 are low and high metastatic potential cell clones derived from lung metastases of the primary tumor. A total of 1,500 proteins was detected. The patterns of protein expression of MTLn2 and MTLn3 cells were similar. Only five spots had a threefold or greater statistically significant difference in staining intensity between MTLn2 and MTLn3 cells, whereas 70 spots differed between MTC and MTLn3 cells. Twenty spots were selected for further study, ten that had a positive correlation of staining intensity with metastatic potential and ten that had a negative (inverse) correlation. Of the 17 unique proteins that were identified, five have often been cited as tumor biomarkers. These included the positive biomarkers nucleophosmin (NPM) and 14-3-3 protein sigma and the negative biomarkers raf kinase inhibitor protein (RKIP), peroxiredoxin-2, and galectin-1. The only identified protein that was markedly higher in MTLn3 cells than in the less-metastatic MTLn2 cells was 14-3-3 protein sigma. The results indicate that increased metastatic potential is associated with positive and negative changes in expression of particular proteins. Proteins that are positively correlated with metastatic potential may prove more useful as clinical biomarkers, but those with negative correlations may still provide useful information about underlying mechanisms of metastatic spread.

Background: Hereditary gingival fibromatosis (HGF) is a fibrotic gingival enlargement. In previous work, HGF fibroblasts grew faster and produced more collagen and fibronectin (FN) than normal gingival (GN) fibroblasts. HGF FN and collagen production, but not proliferation, were under autocrine transforming growth factor (TGF)-beta control, suggesting other means of activation of HGF proliferation. Elevated/prolonged expression of the proto-oncogene c-myc is implicated in disregulation of cell growth. The objectives of this study were to: 1) determine if c-myc expression is abnormal in quiescent and serum-stimulated HGF and GN fibroblasts and 2) determine the relationship between c-myc expression and fibroblast proliferation using a c-myc antisense oligonucleotide (ODN)., Methods: Proliferation was determined by enzyme-linked immunosorbent assay (ELISA), measuring incorporation of bromodeoxyuridine into DNA. Expression of c-myc was determined by quantitative polymerase chain reaction (PCR), using incorporation of fluorescent dCTP and detection via electrophoresis., Results: Proliferation was minimal until 24 hours or more after serum stimulation, when HGF proliferation was greater than GN (P < or = 0.02). All cells expressed c-myc mRNA at quiescence and > or = 1 hour after serum stimulation. Expression of c-myc in quiescent HGF fibroblasts was elevated, and it peaked and remained higher after serum stimulation than in GN cells. Proliferation of an HGF cell line was inhibited by 4 microM c-myc antisense ODN (14% decrease; P < or = 0.006) and 8 microM c-myc antisense ODN (approximately 80% decrease; P < or = 0.0001), but generally not by c-myc sense ODN. This effect was reversed by hybridizing the c-myc antisense and sense ODNs (P = 0.007)., Conclusion: Data suggest that elevated proliferation of an HGF fibroblast cell line is related to elevated c-myc expression.

Background: Previous work showed that normal and aggressive periodontitis (AgP) gingival fibroblasts produce the bone-resorbing cytokine IL-6. PGE2 is important in regulating IL-6 production. Non-steroidal anti-inflammatory drugs inhibit PG synthesis via COX-1 and/or COX-2 isoenzymes and may inhibit periodontal destruction. COX-2 is induced after cellular activation (i.e., by inflammatory cytokines such as IL-1beta). Little is known about IL-1beta-stimulated AgP fibroblast IL-6 and PGE2 production and their regulation by COX inhibitors. The objective of this study was to determine the effects of COX-2 inhibitors on amounts of PGE2 and IL-6 made by IL-1beta-stimulated gingival fibroblasts., Methods: Gingival fibroblasts (2.5 x 10(4)) from healthy or severe periodontitis patients were cultured in serum-free medium, with or without IL-1beta (10(-11)M) for 24 hours, with or without the COX-1/2 inhibitor indomethacin or the selective COX-2 inhibitors NS-398, celecoxib, or rofecoxib. PGE2 and IL-6 in culture supernatants were determined by specific enzyme-linked immunosorbent assay (ELISA)s., Results: All of the COX inhibitors caused dose-dependent decreases in IL-1beta-stimulated PGE2, to a maximum of > 90% in all cell lines (P < or = 0.0001). The selective COX-2 inhibitors, but not indomethacin, caused partial (generally up to approximately 60%), dose-dependent decreases in IL-1beta-stimulated IL-6 in all cell lines (P < or = 0.003). When exogenous PGE2 was added concurrently with COX-2 inhibitors before addition of IL-1beta, IL-6 production returned to levels at or approaching that produced by cells exposed only to IL-1beta (P < or = 0.04)., Conclusion: The results suggest that COX-2 inhibition may be useful in helping to control fibroblast production of IL-6 in patients with severe periodontitis.

Background: Previous work showed that normal and aggressive periodontitis (AgP) gingival fibroblasts produce the boneresorbing cytokine IL-6. PGE 2 is important in regulating IL-6 production. Non-steroidal anti-inflammatory drugs inhibit PG synthesis via COX-1 and/or COX-2 isoenzymes and may inhibit periodontal destruction. COX-2 is induced after cellular activation (i.e., by inflammatory cytokines such as IL-1β). Little is known about IL-1β-stimulated AgP fibroblast IL-6 and PGE 2 production and their regulation by COX inhibitors. The objective of this study was to determine the effects of COX-2 inhibitors on amounts of PGE 2 and IL-6 made by IL-1β-stimulated gingival fibroblasts., Methods: Gingival fibroblasts (2.5 × 10 4 ) from healthy or severe periodontitis patients were cultured in serum-free medium, with or without IL-1β (10 -11 M) for 24 hours, with or without the COX-1/2 inhibitor indomethacin or the selective COX-2 inhibitors NS-398, celecoxib, or rofecoxib. PGE 2 and IL-6 in culture supernatants were determined by specific enzyme-linked immunosorbent assay (ELISA)s., Results: All of the COX inhibitors caused dose-dependent decreases in IL-1β-stimulated PGE 2 , to a maximum of >90% in all cell lines (P ≤0.0001). The selective COX-2 inhibitors, but not indomethacin, caused partial (generally up to approximately 60%), dose-dependent decreases in IL-1β-stimulated IL-6 in all cell lines (P ≤0.003). When exogenous PGE 2 was added concurrently with COX-2 inhibitors before addition of IL-1β, IL-6 production returned to levels at or approaching that produced by cells exposed only to IL-1β (P ≤0.04)., Conclusion: The results suggest that COX-2 inhibition may be useful in helping to control fibroblast production of IL-6 in patients with severe periodontitis. J Periodontol 2003;74:1754-1763., (© 2003 American Academy of Periodontology.)