scholarly journals Cardioprotective Effect of Linalool against Isoproterenol-Induced Myocardial Infarction

Life ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 120
Author(s):  
Maged E. Mohamed ◽  
Mohamed S. Abduldaium ◽  
Nancy S. Younis
Keyword(s):  
Myocardial Infarction ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Antioxidant Activities ◽  
Interleukin 1 ◽  
Cardioprotective Effect ◽  
Cardiac Enzymes ◽  
Necrosis Factor Alpha ◽  
Group Iii ◽  
Apoptotic Markers

Background: Myocardial infarction (MI), a life-threatening disorder, arises from the imbalance between oxygen supply and myocardial demand. Linalool is a naturally occurring monoterpenes with proved numerous pharmacological actions. This study investigated the cardioprotective effect of Linalool on isoproterenol (ISO)-induced MI in rat models and explored part of the underlying molecular mechanisms. Methods: Rats were divided into five groups; groups I and II served as normal and linalool control groups, Group III administered ISO alone; groups V and VI received two different doses of Linalool and were challenged by ISO. Different biochemical parameters were determined, including hemodynamic, infarction size, cardiac enzymes, apoptotic markers, and inflammatory mediators. Results: Linalool limited the infarcted area size and diminished the elevated cardiac enzymes. Linalool escalated HO-1 and Nrf2, both nuclear and cytosol fractions, and reduced Keap 1. Linalool enhanced cardiac antioxidant activities, reduced inflammatory cytokines (tumor necrosis factor-alpha (TNF-α), nuclear factor-κ-B (NF-κB), interleukin 1 beta (IL-1β), interleukin 6 (IL-6)), apoptotic markers (Caspase-3, Caspase-9, and Bax), and elevated Bcl2. Conclusion: Linalool could act as an effective cardioprotective agent in the MI model through improving the oxidative condition, probably via the Nrf2/HO-1 pathway and by abolishing both apoptotic and inflammatory responses.

Efferocytosis during myocardial infarction

2020 ◽  
Vol 168 (1) ◽  
pp. 1-6
Author(s):  
Chikashi Yoshimura ◽  
Akiomi Nagasaka ◽  
Hitoshi Kurose ◽  
Michio Nakaya
Keyword(s):  
Myocardial Infarction ◽  
Cell Death ◽  
Crucial Role ◽  
Molecular Mechanisms ◽  
Causes Of Death ◽  
Inflammatory Responses ◽  
Heart Cells ◽  
Dead Cell ◽  
Related Cell

Abstract Myocardial infarction is one of the major causes of death worldwide. Many heart cells die during myocardial infarction through various processes such as necrosis, apoptosis, necroptosis, autophagy-related cell death, pyroptosis and ferroptosis. These dead cells in infarcted hearts expose the so-called ‘eat-me’ signals, such as phosphatidylserine, on their surfaces, enhancing their removal by professional and non-professional phagocytes. Clearance of dead cells by phagocytes in the diseased hearts plays a crucial role in the pathology of myocardial infarction by inhibiting the inflammatory responses caused by the leakage of contents from dead cells. This review focuses on the rapidly growing understanding of the molecular mechanisms of dead cell phagocytosis, termed efferocytosis, during myocardial infarction, which contributes to the pathophysiology of myocardial infarction.

scholarly journals Development of a lethal model of peritonitis for assessment of laparoscopic and laparotomic treatments in rats

2007 ◽  
Vol 22 (1) ◽  
pp. 39-42 ◽  
Author(s):  
Wilson Salgado Júnior ◽  
José Sebastião dos Santos ◽  
Fernando de Queiroz Cunha
Keyword(s):  
Interleukin 1 ◽  
Cecal Ligation ◽  
Blood Cultures ◽  
Necrosis Factor Alpha ◽  
Group Iii ◽  
Cell Counts ◽  
Group I ◽  
Leukocyte Counts ◽  
Factor Alpha ◽  
Group Ii

PURPOSE: Development of a lethal model of peritonitis to assess the results of treating that peritonitis using videolaparoscopy and laparotomy. METHODS: We developed a model of peritonitis in rats using cecal ligation (CLP) against a 2-mm diameter rigid mold and puncture. Two experiments were performed: determination of seven-day lethality; and analysis of white cell counts, blood cultures and cytokines (Interleukin-1 beta, Tumor Necrosis Factor-alpha and IL-6). The animals were divided into four groups: I - Sham surgery; II - CLP; III - CLP + Videolaparoscopy; and IV- CLP + Laparotomy . RESULTS: Seven-day lethality was 0% in group I, 80% in the group II (p<0.05), 60% in group III , and 20 % in group IV. There was a significant reduction in leukocyte counts and higher levels of serum IL-1 beta, TNF-alpha and IL-6 in the group II compared to controls. The percentages of positive blood cultures were higher after videolaparoscopic compared to laparotomic treatment. CONCLUSION: The experimental model provoked a lethal form of peritonitis and that videolaparoscopic treatment had more bacteraemia than laparotomy.

scholarly journals Macrophage Internalization of Fungal β-Glucans Is Not Necessary for Initiation of Related Inflammatory Responses

2005 ◽  
Vol 73 (10) ◽  
pp. 6340-6349 ◽  
Author(s):  
Frances McCann ◽  
Eva Carmona ◽  
Vishwajeet Puri ◽  
Richard E. Pagano ◽  
Andrew H. Limper
Keyword(s):  
Cell Wall ◽  
Actin Polymerization ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Cytochalasin D ◽  
Fungal Cell ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Phagocytic Cups ◽  
Host Identification

ABSTRACT Cell wall β-glucans are highly conserved structural components of fungi that potently trigger inflammatory responses in an infected host. Identification of molecular mechanisms responsible for internalization and signaling of fungal β-glucans should enhance our understanding of innate immune responses to fungi. In this study, we demonstrated that internalization of fungal β-glucan particles requires actin polymerization but not participation of components of caveolar uptake mechanisms. Using fluorescence microscopy, we observed that uptake of 5-([4,6-dichlorotriazin-2-yl] amino)-fluorescein hydrochloride-Celite complex-labeled Saccharomyces cerevisiae β-glucan by RAW macrophages was substantially reduced in the presence of cytochalasin D, which antagonizes actin-mediated internalization pathways, but not by treatment with nystatin, which blocks caveolar uptake. Interestingly, β-glucan-induced NF-κB translocation, which is necessary for inflammatory activation, and tumor necrosis factor alpha production were both normal in the presence of cytochalasin D, despite defective internalization of β-glucan particles following actin disruption. Dectin-1, a major β-glucan receptor on macrophages, colocalized to phagocytic cups on macrophages and exhibited tyrosine phosphorylation after challenge with β-glucan particles. Dectin-1 localization and other membrane markers were not affected by treatment with cytochalasin D. Furthermore, dectin-1 receptors rather than Toll-like receptor 2 receptors were shown to be necessary for both efficient internalization of β-glucan particles and cytokine release in response to the fungal cell wall component.

Hemoglobin and LPS Act in Synergy to Amplify the Inflammatory Response

2007 ◽  
Vol 86 (9) ◽  
pp. 878-882 ◽  
Author(s):  
C. Bodet ◽  
F. Chandad ◽  
D. Grenier
Keyword(s):  
Gingival Crevicular Fluid ◽  
Inflammatory Responses ◽  
Interleukin 1 ◽  
Fusobacterium Nucleatum ◽  
Necrosis Factor Alpha ◽  
Vascular Disruption ◽  
Tnf Α ◽  
Factor Alpha ◽  
Crevicular Fluid ◽  
Lps Binding

Vascular disruption and bleeding during periodontitis likely increase the levels of hemoglobin in gingival crevicular fluid. The aim of this study was to investigate the effect of hemoglobin on the inflammatory responses of human macrophages stimulated with lipopolysaccharides (LPS) isolated from periodontopathogens. The production of interleukin-1 beta (IL-1β), IL-6, IL-8, and tumor necrosis factor alpha (TNF-α) by macrophages following challenges with Porphyromonas gingivalis and Fusobacterium nucleatum LPS in the presence or absence of human hemoglobin was analyzed by ELISA. The effect of hemoglobin on LPS-binding to macrophages was evaluated with 3H-LPS. Hemoglobin and LPS from periodontopathogens acted in synergy to stimulate the production of high levels of IL-1β, IL-6, IL-8, and TNF-α by macrophages. Hemoglobin also enhanced LPS-binding to macrophages. This study suggests that hemoglobin contributes to increases in the levels of pro-inflammatory mediators in periodontal sites by acting in synergy with LPS from periodontopathogens, thus favoring the progression of periodontitis.

In vivo E-selectin upregulation correlates early with infiltration of PMN, later with PBL entry: MAbs block both

1996 ◽  
Vol 270 (1) ◽  
pp. H183-H193 ◽  
Author(s):  
R. M. Binns ◽  
S. T. Licence ◽  
A. A. Harrison ◽  
E. T. Keelan ◽  
M. K. Robinson ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Interleukin 1 ◽  
Inflammatory Infiltration ◽  
Necrosis Factor Alpha ◽  
Inflammatory Processes ◽  
Factor Alpha ◽  
Kinetics Of ◽  
Necrosis Factor

The endothelial molecule E-selectin binds most leukocyte subsets in vitro. Yet its role in regulating the very different kinetics of inflammatory infiltration of different leukocyte subsets in vivo is unclear. The kinetics of E-selectin upregulation and polymorphonuclear leukocyte (PMN) and blood lymphocyte (PBL) localization in inflammation induced by interleukin-1 alpha (IL-1 alpha), tumor necrosis factor-alpha (TNF-alpha), phytohemagglutinin (PHA), and phorbol myristate acetate (PMA) were investigated in a well-established inbred pig trafficking model. They differed markedly both for these three labeled indicators of inflammation and in each of the four inflammatory processes. In each, E-selectin upregulation correlated with early PMN entry and later with PBL infiltration but was more protracted than both. The importance of E-selectin was confirmed by marked inhibition of PMN and PBL entry (up to > 60%) by F(ab')2 anti-E-selectin. Involvement of other molecules was illustrated by similar or greater inhibition with anti-CD18 F(ab')2. We conclude that, like CD18, E-selectin is necessary for most PMN and PBL infiltration but alone is insufficient, consistent with the involvement of several alternative multistep molecular mechanisms in this entry.

scholarly journals Interleukin-6 Is a Biomarker for the Development of Fatal Severe Acute Respiratory Syndrome Coronavirus 2 Pneumonia

2021 ◽  
Vol 12 ◽  
Author(s):  
André Santa Cruz ◽  
Ana Mendes-Frias ◽  
Ana Isabel Oliveira ◽  
Luís Dias ◽  
Ana Rita Matos ◽  
...  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Inflammatory Responses ◽  
Interleukin 1 ◽  
Binary Logistic Regression ◽  
Significant Negative Correlation ◽  
Peripheral Oxygen Saturation ◽  
Necrosis Factor Alpha ◽  
Reactive Protein ◽  
Arterial Blood ◽  
Disease Stages

Hyper-inflammatory responses induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are a major cause of disease severity and death. Predictive prognosis biomarkers to guide therapeutics are critically lacking. Several studies have indicated a “cytokine storm” with the release of interleukin-1 (IL-1), IL-6, and IL-8, along with tumor necrosis factor alpha (TNFα) and other inflammatory mediators. Here, we proposed to assess the relationship between IL-6 and outcomes of patients with coronavirus disease 2019 (COVID-19). Our cohort consisted of 46 adult patients with PCR-proven SARS-CoV-2 infection admitted in a COVID-19 ward of the Hospital de Braga (HB) from April 7 to May 7, 2020, whose IL-6 levels were followed over time. We found that IL-6 levels were significantly different between the disease stages. Also, we found a significant negative correlation between IL-6 levels during stages IIb and III, peripheral oxygen saturation (SpO2), and partial pressure of oxygen in arterial blood (PaO2), showing that IL-6 correlates with respiratory failure. Compared to the inflammatory markers available in the clinic routine, we found a positive correlation between IL-6 and C-reactive protein (CRP). However, when we assessed the predictive value of these two markers, IL-6 behaves as a better predictor of disease progression. In a binary logistic regression, IL-6 level was the most significant predictor of the non-survivors group, when compared to age and CRP. Herein, we present IL-6 as a relevant tool for prognostic evaluation, mainly as a predictor of outcome.

scholarly journals Targeting Cytokines for Morphine Tolerance: A Narrative Review

2019 ◽  
Vol 17 (4) ◽  
pp. 366-376 ◽  
Author(s):  
Dai-Qiang Liu ◽  
Ya-Qun Zhou ◽  
Feng Gao
Keyword(s):  
Side Effects ◽  
Molecular Mechanisms ◽  
Interleukin 1 ◽  
Morphine Tolerance ◽  
Interleukin 10 ◽  
Medical Subject Headings ◽  
Potent Effect ◽  
Necrosis Factor Alpha ◽  
Pubmed Database ◽  
Factor Alpha

Background:Despite its various side effects, morphine has been widely used in clinics for decades due to its powerful analgesic effect. Morphine tolerance is one of the major side effects, hindering its long-term usage for pain therapy. Currently, the thorough cellular and molecular mechanisms underlying morphine tolerance remain largely uncertain.Methods:We searched the PubMed database with Medical subject headings (MeSH) including ‘morphine tolerance’, ‘cytokines’, ‘interleukin 1’, ‘interleukin 1 beta’, ‘interleukin 6’, ‘tumor necrosis factor alpha’, ‘interleukin 10’, ‘chemokines’. Manual searching was carried out by reviewing the reference lists of relevant studies obtained from the primary search. The searches covered the period from inception to November 1, 2017.Results:The expression levels of certain chemokines and pro-inflammatory cytokines were significantly increased in animal models of morphine tolerance. Cytokines and cytokine receptor antagonist showed potent effect of alleviating the development of morphine tolerance.Conclusion:Cytokines play a fundamental role in the development of morphine tolerance. Therapeutics targeting cytokines may become alternative strategies for the management of morphine tolerance.

scholarly journals AP-1/IRF-3 Targeted Anti-Inflammatory Activity of Andrographolide Isolated fromAndrographis paniculata

2013 ◽  
Vol 2013 ◽  
pp. 1-16 ◽  
Author(s):  
Ting Shen ◽  
Woo Seok Yang ◽  
Young-Su Yi ◽  
Gi-Ho Sung ◽  
Man Hee Rhee ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Peritoneal Macrophages ◽  
Luciferase Reporter ◽  
Prostaglandin E ◽  
Dependent Manner ◽  
Molecular Signaling ◽  
Luciferase Reporter Gene ◽  
Necrosis Factor Alpha ◽  
Anti Inflammatory

Andrographolide (AG) is an abundant component of plants of the genusAndrographisand has a number of beneficial properties including neuroprotective, anticancer, anti-inflammatory, and antidiabetic effects. Despite numerous pharmacological studies, the precise mechanism of AG is still ambiguous. Thus, in the present study, we investigated the molecular mechanisms of AG and its target proteins as they pertain to anti-inflammatory responses. AG suppressed the production of nitric oxide (NO) and prostaglandin E2(PGE2), as well as the mRNA abundance of inducible NO synthase (iNOS), tumor necrosis factor-alpha (TNF-α), cyclooxygenase (COX)-2, and interferon-beta (IFN-β) in a dose-dependent manner in both lipopolysaccharide- (LPS-) activated RAW264.7 cells and peritoneal macrophages. AG also substantially ameliorated the symptoms of LPS-induced hepatitis and EtOH/HCl-induced gastritis in mice. Based on the results of luciferase reporter gene assays, kinase assays, and measurement of nuclear levels of transcription factors, the anti-inflammatory effects of AG were found to be clearly mediated by inhibition of both (1) extracellular signal-regulated kinase (ERK)/activator protein (AP)-1 and (2) IκB kinaseε(IKKε)/interferon regulatory factor (IRF)-3 pathways. In conclusion, we detected a novel molecular signaling pathway by which AG can suppress inflammatory responses. Thus, AG is a promising anti-inflammatory drug with two pharmacological targets.

scholarly journals Molecular Characterization of the Acute Inflammatory Response to Infections with Gram-Negative versus Gram-Positive Bacteria

2003 ◽  
Vol 71 (10) ◽  
pp. 5803-5813 ◽  
Author(s):  
Robert J. Feezor ◽  
Caroline Oberholzer ◽  
Henry V. Baker ◽  
Daniela Novick ◽  
Menachem Rubinstein ◽  
...  
Keyword(s):  
Whole Blood ◽  
Inflammatory Responses ◽  
Ex Vivo ◽  
Interleukin 1 ◽  
Gram Negative Bacteria ◽  
Gram Positive ◽  
Blood Leukocytes ◽  
Necrosis Factor Alpha ◽  
Gram Negative ◽  
Gram Positive Bacteria

ABSTRACT Sepsis caused by gram-negative bacteria and that caused by gram-positive bacteria often manifest similar clinical features. We investigated plasma proinflammatory cytokine profiles in patients with sepsis due to gram-positive and gram-negative bacteria and studied the cytokine production and differential gene regulation of leukocytes stimulated ex vivo with Escherichia coli lipopolysaccharide or heat-killed Staphylococcus aureus. Concentrations of tumor necrosis factor alpha, interleukin 1 receptor antagonist (IL-1Ra), IL-8, IL-10, IL-18 binding protein, procalcitonin, and protein C in plasma did not differ between patients with sepsis due to gram-negative and gram-positive bacteria. However, plasma IL-1β, IL-6, and IL-18 concentrations were significantly higher in patients with sepsis due to gram-positive bacteria. Ex vivo stimulation of whole blood with heat-killed S. aureus markedly increased IL-1β and IL-18 levels more than E. coli lipopolysaccharide stimulation. Microarray analysis revealed at least 359 cross-validated probe sets (genes) significant at the P < 0.001 level whose expression discriminated among gram-negative-organism-stimulated, gram-positive-organism-stimulated, and unstimulated whole-blood leukocytes. The host inflammatory responses to gram-negative and gram-positive stimuli share some common response elements but also exhibit distinct patterns of cytokine appearance and leukocyte gene expression.

scholarly journals IKKβ-Targeted Anti-Inflammatory Activities of a Butanol Fraction of Artificially CultivatedCordyceps pruinosaFruit Bodies

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Han Gyung Kim ◽  
Woo Seok Yang ◽  
Gi-Ho Sung ◽  
Ji Hye Kim ◽  
Gwang-Soo Baek ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Immunoblot Analysis ◽  
Culture Conditions ◽  
Gastric Ulcers ◽  
Luciferase Reporter ◽  
Necrosis Factor Alpha ◽  
Butanol Fraction ◽  
Reporter Assays ◽  
Anti Inflammatory

The inhibitory activities of theCordyceps pruinosabutanol fraction (Cp-BF) were investigated by determining inflammatory responses of lipopolysaccharide (LPS)-treated RAW264.7 macrophage cells and by evaluating HCl/ethanol (EtOH)-triggered gastric ulcers in mice. The molecular mechanisms of the inhibitory effects of Cp-BF were investigated by identifying target enzymes using biochemical and molecular biological approaches. Cp-BF strongly inhibited the production of NO and TNF-α, release of reactive oxygen species (ROS), phagocytic uptake of FITC-dextran, and mRNA expression levels of interleukin (IL)-6, inducible NO synthase (iNOS), and tumour necrosis factor-alpha (TNF)-αin activated RAW264.7 cells. Cp-BF also strongly downregulated the NF-κB pathway by suppressing IKKβaccording to luciferase reporter assays and immunoblot analysis. Furthermore, Cp-BF blocked both increased levels of NF-κB-mediated luciferase activities and phosphorylation of p65/p50 observed by IKKβoverexpression. Finally, orally administered Cp-BF was found to attenuate gastric ulcer and block the phosphorylation of IκBαinduced by HCl/EtOH. Therefore, these results suggest that the anti-inflammatory activity of Cp-BF may be mediated by suppression of IKKαand its downstream NF-κB activation. Since our group has established the mass cultivation conditions by developing culture conditions forCordyceps pruinosa, the information presented in this study may be useful for developing new anti-inflammatory agents.

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