scholarly journals Essential Oils and Their Major Compounds in the Treatment of Chronic Inflammation: A Review of Antioxidant Potential in Preclinical Studies and Molecular Mechanisms

2018 ◽  
Vol 2018 ◽  
pp. 1-23 ◽  
Author(s):  
Érica Martins de Lavor ◽  
Antônio Wilton Cavalcante Fernandes ◽  
Roxana Braga de Andrade Teles ◽  
Ana Ediléia Barbosa Pereira Leal ◽  
Raimundo Gonçalves de Oliveira Júnior ◽  
...  
Keyword(s):  
Essential Oils ◽  
Chronic Inflammation ◽  
Molecular Mechanisms ◽  
Inflammatory Diseases ◽  
Biologically Active ◽  
Preclinical Studies ◽  
Inflammatory Conditions ◽  
Potential Activity

Inflammatory diseases result from the body’s response to tissue damage, and if the resolution is not adequate or the stimulus persists, there will be progression from acute inflammation to chronic inflammation, leading to the development of cancer and neurodegenerative and autoimmune diseases. Due to the complexity of events that occur in inflammation associated with the adverse effects of drugs used in clinical practice, it is necessary to search for new biologically active compounds with anti-inflammatory activity. Among natural products, essential oils (EOs) present promising results in preclinical studies, with action in the main mechanisms involved in the pathology of inflammation. The present systematic review summarizes the pharmacological effects of EOs and their compounds in in vitro and in vivo models for inflammation. The research was conducted in the following databases: PubMed, Scopus, BIREME, Scielo, Open Grey, and Science Direct. Based on the inclusion criteria, 30 articles were selected and discussed in this review. The studies listed revealed a potential activity of EOs and their compounds for the treatment of inflammatory diseases, especially in chronic inflammatory conditions, with the main mechanism involving reduction of reactive oxygen and nitrogen species associated with an elevation of antioxidant enzymes as well as the reduction of the nuclear factor kappa B (NF-κB), reducing the expression of proinflammatory cytokines. Thus, this review suggests that EOs and their major compounds are promising tools for the treatment of chronic inflammation.

scholarly journals Comparative investigation of sesquiterpene components of essential oils originating from intact plants and hairy root chamomile cultures

2021 ◽  
Vol 6 (2) ◽  
pp. 028-049
Author(s):  
Éva Szőke ◽  
Éva Lemberkovics
Keyword(s):  
Essential Oil ◽  
Essential Oils ◽  
Hairy Root ◽  
Folk Medicine ◽  
Root Culture ◽  
Hairy Root Culture ◽  
Comparative Investigation ◽  
Biologically Active

The importance of chamomile (Chamomilla recutita) inflorescence is widely known in classical and folk medicine, with the largest group of its effective constituents forming the essential oil (chamazulene, a-bisabolol, α-farnesene, trans-β-farnesene, spathulenol, cis/trans-en-in-dicycloethers). Among cultivated species, the Hungarian BK-2 contains more chamazulene in its essential oil than the German Degumil type, which is mainly cultivated for its a-bisabolol. Both components have important antiinflammatory activities. Wild populations can be easily distinguished from cultivated ones by their high amount of bisaboloides, particularly the flower of Hungarian Szabadkígyós wild type, which contained on average 48 % of the biologically active (-)-a-bisabolol. The population of Szabadkígyós has good salt tolerance which is important owing to global warming, because the proportion of saline areas is increasing worldwide. To keep the genome of Szabadkígyós having high (-)-a-bisabolol content, Szőke and research team used biotechnological methods. Sterile plantlets, were infected by Agrobacterium rhizogenes strains #A-4, #15834, #R-1601. The hairy root clones possessing the best growing and biosynthetical potential were multiplied for phytochemical investigations. Pharmacologically important compounds of their essential oils were followed in great detail. The amount of in vitro cultured terpenoids and polyin compounds was compared with that of in vivo plants. GC-MS studies showed that sterile chamomile cultures generated the most important terpenoid and polyin compounds characteristics of the mother plant. Berkheyaradulene, geranyl-isovalerat and cedrol as new components were identified in these sterile cultures. The main component of hairy root cultures (D/400, D/1, D/100 and Sz/400) was tr-b-farnesene and in addition one new compound: a-selinene was identified. Hairy root culture originated from chamomile collected in Szabadkígyós was intensive increased the essential oil content and pharmacological active compounds: (-) -α-bisabolol and β-eudesmol was also synthetized in large quantity. Furthermore, in vitro organized cultures were made from this population to obtain propagation material containing numerous active substances.

scholarly journals Current translational potential and underlying molecular mechanisms of necroptosis

2019 ◽  
Vol 10 (11) ◽  
Author(s):  
Tamás Molnár ◽  
Anett Mázló ◽  
Vera Tslaf ◽  
Attila Gábor Szöllősi ◽  
Gabriella Emri ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Posttranslational Modifications ◽  
Molecular Mechanisms ◽  
Inflammatory Diseases ◽  
Immune Surveillance ◽  
Kinase Domain ◽  
Tumor Formation

Abstract Cell death has a fundamental impact on the evolution of degenerative disorders, autoimmune processes, inflammatory diseases, tumor formation and immune surveillance. Over the past couple of decades extensive studies have uncovered novel cell death pathways, which are independent of apoptosis. Among these is necroptosis, a tightly regulated, inflammatory form of cell death. Necroptosis contribute to the pathogenesis of many diseases and in this review, we will focus exclusively on necroptosis in humans. Necroptosis is considered a backup mechanism of apoptosis, but the in vivo appearance of necroptosis indicates that both caspase-mediated and caspase-independent mechanisms control necroptosis. Necroptosis is regulated on multiple levels, from the transcription, to the stability and posttranslational modifications of the necrosome components, to the availability of molecular interaction partners and the localization of receptor-interacting serine/threonine-protein kinase 1 (RIPK1), receptor-interacting serine/threonine-protein kinase 3 (RIPK3) and mixed lineage kinase domain-like protein (MLKL). Accordingly, we classified the role of more than seventy molecules in necroptotic signaling based on consistent in vitro or in vivo evidence to understand the molecular background of necroptosis and to find opportunities where regulating the intensity and the modality of cell death could be exploited in clinical interventions. Necroptosis specific inhibitors are under development, but >20 drugs, already used in the treatment of various diseases, have the potential to regulate necroptosis. By listing necroptosis-modulated human diseases and cataloging the currently available drug-repertoire to modify necroptosis intensity, we hope to kick-start approaches with immediate translational potential. We also indicate where necroptosis regulating capacity should be considered in the current applications of these drugs.

Role of macrophage CD44 in the disposal of inflammatory cell corpses*

2002 ◽  
Vol 103 (5) ◽  
pp. 441-449 ◽  
Author(s):  
Sharon VIVERS ◽  
Ian DRANSFIELD ◽  
Simon P. HART
Keyword(s):  
Molecular Mechanisms ◽  
Inflammatory Diseases ◽  
Surrounding Tissue ◽  
Human Macrophage ◽  
Neutrophil Granulocytes ◽  
Apoptotic Cells ◽  
Tissue Destruction

Understanding the cellular and molecular mechanisms that determine whether inflammation resolves or progresses to scarring and tissue destruction should lead to the development of effective therapeutic strategies for inflammatory diseases. Apoptosis of neutrophil granulocytes is an important determinant of the resolution of inflammation, providing a mechanism for down-regulation of function and triggering clearance by macrophages without inducing a pro-inflammatory response. However, if the rate of cell death by apoptosis is such that the macrophage clearance capacity is exceeded, apoptotic cells may progress to secondary necrosis, resulting in the release of harmful cellular contents and in damage to the surrounding tissue. There are many possible ways in which the rate and capacity of the macrophage-mediated clearance of apoptotic cells may be enhanced or suppressed. Ligation of human macrophage surface CD44 by bivalent monoclonal antibodies rapidly and profoundly augments the capacity of macrophages to phagocytose apoptotic neutrophils in vitro. The molecular mechanism behind this effect and its potential significance in vivo is a current focus of research.

scholarly journals Bee Venom: From Venom to Drug

Molecules ◽  
2021 ◽  
Vol 26 (16) ◽  
pp. 4941
Author(s):  
Abdelwahab Khalil ◽  
Basem H. Elesawy ◽  
Tarek M. Ali ◽  
Osama M. Ahmed
Keyword(s):  
Molecular Mechanisms ◽  
Biological Activities ◽  
Biologically Active ◽  
Bee Venom ◽  
Bee Sting ◽  
Anti Cancer ◽  
Defensive Substance ◽  
Injectable Form

Insects of the order Hymenoptera have a defensive substance that contains many biologically active compounds. Specifically, venom from honeybees (Apis mellifera) contains many enzymes and peptides that are effective against various diseases. Different research papers stated the possibility of using bee venom (a direct bee sting or in an injectable form) in treating several complications; either in vivo or in vitro. Other reports used the active fractions of bee venom clinically or at labratory scale. Many reports and publications have stated that bee venom and its constituents have multiple biological activities including anti-microbial, anti-protozoan, anti-cancer, anti-inflammatory, and anti-arthritic properties. The present review aims to refer to the use of bee venom itself or its fractions in treating several diseases and counteracting drug toxicities as an alternative protocol of therapy. The updated molecular mechanisms of actions of bee venom and its components are discussed in light of the previous updated publications. The review also summarizes the potential of venom loaded on nanoparticles as a drug delivery vehicle and its molecular mechanisms. Finally, the products of bee venom available in markets are also demonstrated.

scholarly journals Dissociated Steroids

2007 ◽  
Vol 7 ◽  
pp. 421-430 ◽  
Author(s):  
Matthew C. Catley
Keyword(s):  
Side Effects ◽  
Molecular Mechanisms ◽  
Inflammatory Diseases ◽  
Therapeutic Index ◽  
Clinical Use ◽  
Response Elements ◽  
Activation Of Transcription

Glucocorticoids (GCs) are some of the most important drugs in clinical use today. They are mainly used to suppress disease-related inflammation and are widely used for the treatment of many inflammatory diseases including asthma and arthritis. However, GCs are also associated with debilitating side effects that place limitations on the long-term use of these drugs. The development of a GC with reduced side effects would allow more effective treatments for patients who require long-term suppression of inflammation. GCs exert their effects by binding and activating the GC receptor (GR). The activated receptor then binds GC response elements (GREs) in the promoter of genes, and activates transcription (transactivation) or interferes with the activation of transcription by inhibiting the transactivating function of other transcription factors, such as AP-1 and NF-ĸB (transrepression). Transrepression is believed to be responsible for the majority of the beneficial anti-inflammatory effects of GCs, whereas transactivation is believed to play a bigger role in the unwanted side effects of GCs. Compounds that can dissociate the transactivation function of GCs from the transrepression function may, therefore, have an improved therapeutic index. A number of these dissociated corticosteroids have been developed.In vitroassays using these compounds appear to show good dissociation. However,in vivo, the dissociation appears to be lost and these compounds still produce many of the side effects associated with conventional GCs. A better understanding of the molecular mechanisms behind GC-induced effects would allow the design of novel selective GR modulators with an improved therapeutic index.

scholarly journals Control of Erythropoiesis in Rats With Adjuvant-induced Chronic Inflammation

Blood ◽  
1973 ◽  
Vol 41 (1) ◽  
pp. 37-44 ◽  
Author(s):  
John N. Lukens
Keyword(s):  
Chronic Inflammation ◽  
Barometric Pressure ◽  
Biologically Active ◽  
Endogenous Erythropoietin ◽  
Adjuvant Disease ◽  
Disease Exposure ◽  
The Relationship ◽  
Erythropoietic Response

Abstract In order to characterize the defect in erythroid homeostasis in chronic inflammatory states, the relationship between erythropoietin production and erythropoietic response was examined in rats with adjuvant disease. Exposure of adjuvant-injected rats to graded levels of lowered barometric pressure induced increases in plasma erythropoietin which were significantly less than those measured in normal animals similarly stimulated. Erythropoietin inhibitors were not detected by in vitro or in vivo assay techniques: the biological activity of ovine erythropoietin was not modified by incubation with plasma from rats with adjuvant disease; the erythropoietic response of ex-hypoxic polycythemic mice to erythropoietin was not compromised by injections of test plasma; and the burst of erythropoiesis induced in ex-hypoxic polycythemic mice by a hypobaric stimulus was not modified by plasma given prior to or at various intervals after hypobaric exposure. Exogenous erythropoietin elicited nearly identical increases of radioiron incorporation in normal and adjuvant-injected rats whose endogenous erythropoietin was suppressed by hypertransfusion. It is concluded that the diminished erythropoietic response to anemia in adjuvant-induced chronic inflammation results from a relative failure in the production of biologically active erythropoietin.

scholarly journals The Transcription Factor MAFF Regulates an Atherosclerosis Relevant Network Connecting Inflammation and Cholesterol Metabolism

Circulation ◽  
2021 ◽  
Author(s):  
Moritz von Scheidt ◽  
Yuqi Zhao ◽  
Thomas Q. de Aguiar Vallim ◽  
Nam Che ◽  
Michael Wierer ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Molecular Mechanisms ◽  
Prediction Models ◽  
Cholesterol Metabolism ◽  
Association Studies ◽  
Experimental Studies ◽  
Genome Wide Association Studies ◽  
Inflammatory Conditions

Background: Coronary artery disease (CAD) is a multifactorial condition with both genetic and exogenous causes. The contribution of tissue specific functional networks to the development of atherosclerosis remains largely unclear. The aim of this study was to identify and characterise central regulators and networks leading to atherosclerosis. Methods: Based on several hundred genes known to affect atherosclerosis risk in mouse (as demonstrated in knock-out models) and human (as shown by genome-wide association studies (GWAS)) liver gene regulatory networks were modeled. The hierarchical order and regulatory directions of genes within the network were based on Bayesian prediction models as well as experimental studies including chromatin immunoprecipitation DNA-Sequencing (ChIP-Seq), ChIP mass spectrometry (ChIP-MS), overexpression, siRNA knockdown in mouse and human liver cells, and knockout mouse experiments. Bioinformatics and correlation analyses were used to clarify associations between central genes and CAD phenotypes in both human and mouse. Results: The transcription factor MAFF interacted as a key driver of a liver network with three human genes at CAD GWAS loci and eleven atherosclerotic murine genes. Most importantly, expression levels of the low-density lipoprotein receptor ( LDLR ) gene correlated with MAFF in 600 CAD patients undergoing bypass surgery (STARNET) and a hybrid mouse diversity panel involving 105 different inbred mouse strains. Molecular mechanisms of MAFF were tested under non-inflammatory conditions showing a positive correlation between MAFF and LDLR in vitro and in vivo . Interestingly, after LPS stimulation (inflammatory conditions) an inverse correlation between MAFF and LDLR in vitro and in vivo was observed. ChIP-MS revealed that the human CAD GWAS candidate BACH1 assists MAFF in the presence of LPS stimulation with respective heterodimers binding at the MAF recognition element (MARE) of the LDLR promoter to transcriptionally downregulate LDLR expression. Conclusions: The transcription factor MAFF was identified as a novel central regulator of an atherosclerosis/CAD relevant liver network. MAFF triggered context specific expression of LDLR and other genes known to affect CAD risk. Our results suggest that MAFF is a missing link between inflammation, lipid and lipoprotein metabolism and a possible treatment target.

scholarly journals Sex Specific Determinants in Osteoarthritis: A Systematic Review of Preclinical Studies

2020 ◽  
Vol 21 (10) ◽  
pp. 3696 ◽  
Author(s):  
Deyanira Contartese ◽  
Matilde Tschon ◽  
Monica De Mattei ◽  
Milena Fini
Keyword(s):  
Gene Expression ◽  
Systematic Review ◽  
Sex Differences ◽  
Animal Models ◽  
Molecular Mechanisms ◽  
Joint Disease ◽  
In Vivo Studies ◽  
Preclinical Studies

Osteoarthritis (OA) is a highly prevalent joint disease that primarily affects about 10% of the world’s population over 60 years old. The purpose of this study is to systematically review the preclinical studies regarding sex differences in OA, with particular attention to the molecular aspect and gene expression, but also to the histopathological aspects. Three databases (PubMed, Scopus, and Web of Knowledge) were screened for eligible studies. In vitro and in vivo papers written in English, published in the last 11 years (2009–2020) were eligible. Participants were preclinical studies, including cell cultures and animal models of OA, evaluating sex differences. Independent extraction of articles and quality assessments were performed by two authors using predefined data fields and specific tools (Animals in Research Reporting In Vivo Experiments (ARRIVE) guideline and Systematic Review Centre for Laboratory animal Experimentation (SYRCLE) tool). Twenty-three studies were included in the review: 4 in vitro studies, 18 in vivo studies, and 1 both in vitro and in vivo study. From in vitro works, sex differences were found in the gene expression of inflammatory molecules, hormonal receptors, and in responsiveness to hormonal stimulation. In vivo research showed a great heterogeneity of animal models mainly focused on the histopathological aspects rather than on the analysis of sex-related molecular mechanisms. This review highlights that many gaps in knowledge still exist; improvementsin the selection and reporting of animal models, the use of advanced in vitro models, and multiomics analyses might contribute to developing a personalized gender-based medicine.

scholarly journals Anti-Inflammatory Effects of GLP-1-Based Therapies beyond Glucose Control

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Young-Sun Lee ◽  
Hee-Sook Jun
Keyword(s):  
Pancreatic Beta Cells ◽  
Molecular Mechanisms ◽  
Inflammatory Diseases ◽  
Glucose Disposal ◽  
Dipeptidyl Peptidase 4 ◽  
Beneficial Effects ◽  
Anti Inflammatory ◽  
Glucagon Like Peptide 1

Glucagon-like peptide-1 (GLP-1) is an incretin hormone mainly secreted from intestinal L cells in response to nutrient ingestion. GLP-1 has beneficial effects for glucose homeostasis by stimulating insulin secretion from pancreatic beta-cells, delaying gastric emptying, decreasing plasma glucagon, reducing food intake, and stimulating glucose disposal. Therefore, GLP-1-based therapies such as GLP-1 receptor agonists and inhibitors of dipeptidyl peptidase-4, which is a GLP-1 inactivating enzyme, have been developed for treatment of type 2 diabetes. In addition to glucose-lowering effects, emerging data suggests that GLP-1-based therapies also show anti-inflammatory effects in chronic inflammatory diseases including type 1 and 2 diabetes, atherosclerosis, neurodegenerative disorders, nonalcoholic steatohepatitis, diabetic nephropathy, asthma, and psoriasis. This review outlines the anti-inflammatory actions of GLP-1-based therapies on diseases associated with chronic inflammationin vivoandin vitro, and their molecular mechanisms of anti-inflammatory action.

scholarly journals A mouse model of human TLR4 D299G/T399I SNPs reveals mechanisms of altered LPS and pathogen responses

2020 ◽  
Vol 218 (2) ◽  
Author(s):  
Katharina Richard ◽  
Kurt H. Piepenbrink ◽  
Kari Ann Shirey ◽  
Archana Gopalakrishnan ◽  
Shreeram Nallar ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Inflammatory Diseases ◽  
Differential Susceptibility ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Tlr4 Signaling ◽  
The Impact ◽  
Signaling Efficiency

Two cosegregating single-nucleotide polymorphisms (SNPs) in human TLR4, an A896G transition at SNP rs4986790 (D299G) and a C1196T transition at SNP rs4986791 (T399I), have been associated with LPS hyporesponsiveness and differential susceptibility to many infectious or inflammatory diseases. However, many studies failed to confirm these associations, and transfection experiments resulted in conflicting conclusions about the impact of these SNPs on TLR4 signaling. Using advanced protein modeling from crystallographic data of human and murine TLR4, we identified homologous substitutions of these SNPs in murine Tlr4, engineered a knock-in strain expressing the D298G and N397I TLR4 SNPs homozygously, and characterized in vivo and in vitro responses to TLR4 ligands and infections in which TLR4 is implicated. Our data provide new insights into cellular and molecular mechanisms by which these SNPs decrease the TLR4 signaling efficiency and offer an experimental approach to confirm or refute human data possibly confounded by variables unrelated to the direct effects of the SNPs on TLR4 functionality.

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