scholarly journals Chenopodium ambrosioides L. Improves Phagocytic Activity and Decreases Bacterial Growth and the Systemic Inflammatory Response in Sepsis Induced by Cecal Ligation and Puncture

2017 ◽  
Vol 8 ◽  
Author(s):  
Carlos E. P. Rios ◽  
Afonso G. Abreu ◽  
Jose A. F. Braga Filho ◽  
Johnny R. Nascimento ◽  
Rosane N. M. Guerra ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Bacterial Growth ◽  
Phagocytic Activity ◽  
Cecal Ligation ◽  
Systemic Inflammatory Response ◽  
Cecal Ligation And Puncture ◽  
Chenopodium Ambrosioides

scholarly journals Hydrogen Gas Presents a Promising Therapeutic Strategy for Sepsis

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Keliang Xie ◽  
Lingling Liu ◽  
Yonghao Yu ◽  
Guolin Wang
Keyword(s):  
Inflammatory Response ◽  
Molecular Hydrogen ◽  
Therapeutic Strategy ◽  
Cecal Ligation ◽  
Organ Damage ◽  
Hydrogen Gas ◽  
Diagnostic Tools ◽  
Hydrogen Treatment ◽  
Cecal Ligation And Puncture ◽  
Monitoring Devices

Sepsis is characterized by a severe inflammatory response to infection. It remains a major cause of morbidity and mortality in critically ill patients despite developments in monitoring devices, diagnostic tools, and new therapeutic options. Recently, some studies have found that molecular hydrogen is a new therapeutic gas. Our studies have found that hydrogen gas can improve the survival and organ damage in mice and rats with cecal ligation and puncture, zymosan, and lipopolysaccharide-induced sepsis. The mechanisms are associated with the regulation of oxidative stress, inflammatory response, and apoptosis, which might be through NF-κB and Nrf2/HO-1 signaling pathway. In this paper, we summarized the progress of hydrogen treatment in sepsis.

COMPARISON OF THE MORTALITY AND INFLAMMATORY RESPONSE OF TWO MODELS OF SEPSIS: LIPOPOLYSACCHARIDE VS. CECAL LIGATION AND PUNCTURE

Shock ◽  
2000 ◽  
Vol 13 (2) ◽  
pp. 110-116 ◽  
Author(s):  
Daniel G. Remick ◽  
David E. Newcomb ◽  
Gerald L. Bolgos ◽  
Douglas R. Call
Keyword(s):  
Inflammatory Response ◽  
Cecal Ligation ◽  
Cecal Ligation And Puncture

scholarly journals Hemodynamic evaluation of chemical mediators of sepsis during systemic inflammatory response in an experimental animal model

2021 ◽  
Author(s):  
GUILHERME DE SOUZA VIEIRA ◽  
Fernanda Antunes ◽  
Josias Alves Machado ◽  
Isabella Cristina Morales ◽  
Priscilla Olivieri Benck de Jesus ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Inflammatory Response ◽  
Arterial Blood Pressure ◽  
Cecal Ligation ◽  
Systemic Inflammatory Response ◽  
Arterial Blood ◽  
Time Period ◽  
Sepsis Induction ◽  
Surgical Manipulation

The early diagnosis of sepsis increases the chances of its successful treatment. Biomarkers are able to distinguish between systemic inflammatory response syndrome and sepsis and are used to monitor pro- and anti-inflammatory changes associated with the host response to pathogens. A total of 11 rats underwent sepsis induction and measured systolic, diastolic and mean arterial blood pressure. Leukocyte counts, procalcitonin, and nitric oxide also were measured 0, 2, and 4 hours after the induction of sepsis using the cecal ligation and puncture method. The animals were divided into two groups: control (SHAM) and induced. Procalcitonin levels remained within the normal range for an inflammatory response throughout the experiment. There was a statistically insignificant increase in nitric oxide levels. All animals showed increased diastolic arterial blood pressure; however, the increase in the induced animals was even more pronounced. Procalcitonin and nitric oxide levels can increase due to surgical manipulation, while arterial blood pressure was not a good predictor for the onset of sepsis during the time period studied here.

scholarly journals Inhibition of Gamma Interferon Decreases Bacterial Load in Peritonitis by Accelerating Peritoneal Fibrin Deposition and Tissue Repair

2003 ◽  
Vol 71 (5) ◽  
pp. 2766-2774 ◽  
Author(s):  
Gang Qiu ◽  
Elizabeth Gribbin ◽  
Kathryn Harrison ◽  
Neil Sinha ◽  
Kingsley Yin
Keyword(s):  
Inflammatory Response ◽  
Tissue Repair ◽  
Bowel Perforation ◽  
Bacterial Load ◽  
Cecal Ligation ◽  
Gamma Interferon ◽  
Systemic Inflammatory Response ◽  
Fibrin Deposition ◽  
Septic Peritonitis ◽  
Ifn Γ

ABSTRACT Bowel perforation can lead to significant bacterial spillage, which may then cause septic peritonitis, characterized by a systemic inflammatory response and organ dysfunction. There are several reports that have shown that the development of peritoneal adhesions is dependent on inflammatory cytokine levels and that these adhesions can reduce bacterial spread, possibly by sealing off the cecum in the cecal ligation and puncture (CLP) model of septic peritonitis. There have not, however, been any studies that have utilized a strategy to accelerate tissue repair in order to seal off the injured cecum and reduce bacterial spread as well as ameliorate systemic inflammation. In the present study, we demonstrate that the administration of anti-gamma interferon (IFN-γ) antibody (1.2 mg/kg of body weight, intravenously) accelerated tissue repair via increased fibrin deposition 12 and 24 h after CLP in rats. This increase in fibrin deposition was associated with peritoneal adhesion 24 h after CLP and a reduction in bacterial load compared to the bacterial load of rats given irrelevant antibody. Plasma fibrin levels, however, were not altered after IFN-γ antibody administration, suggesting that the inhibition of IFN-γ activity specifically increased fibrin deposition to the site of injury. Furthermore, plasma interleukin-6, used as a marker of systemic inflammatory response, was reduced in CLP rats given IFN-γ antibody compared to that found in those given irrelevant antibody. These results suggest that the early inhibition of IFN-γ activity in the CLP model is beneficial by accelerating fibrin deposition in cecal tissue to prevent bacterial spread and reduce the systemic inflammatory response. Importantly, increased fibrin deposition in the ceca was not associated with increased plasma fibrin whereas the latter may have detrimental effects associated with coagulation disorders.

scholarly journals Protein from Hevea brasiliensis “Hev b 13” latex attenuates systemic inflammatory response and lung lesions in rats with sepsis

2017 ◽  
Vol 78 (2) ◽  
pp. 271-280 ◽  
Author(s):  
L. A. Araújo ◽  
P. R. Melo-Reis ◽  
F. Mrue ◽  
C. M. Gomes ◽  
M. A. P. Oliveira ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Hevea Brasiliensis ◽  
Rubber Tree ◽  
Cecal Ligation ◽  
Neutrophil Infiltration ◽  
Multiple Organ ◽  
Systemic Inflammatory Response ◽  
Lung Lesions ◽  
Male Wistar Rats ◽  
Anti Inflammatory

Abstract Sepsis induces a severe systemic inflammatory response that may result in multiple organ dysfunction and death. Studies using a protein derived from natural Hevea brasiliensis (rubber tree) latex, denominated Hev b 13, have demonstrated important anti-inflammatory effects, but no data have been published regarding its effects on sepsis. The aim of this study was to investigate the effects of Hev b 13 on the inflammatory response and lung lesions of septal rats. Male Wistar rats were submitted to cecal ligation and puncture (CLP), randomized into groups and treated with subcutaneously administered doses of 0.5/2.0/3.0 mg/Kg of Hev b 13. Next, animals were subdivided into three different points in time (1, 6 and 24 hours after treatments) for collection of blood samples and euthanasia accompanied by organ removal. Total and differential leukocyte counts, cytokine dosage and histological assessment were analyzed. Treatment with Hev b 13 resulted in a significant decline in total and differential leukocytes as well as suppression of TNF-α and IL-6 production, associated with the increase in IL-10 and IL-4 in plasma and lung tissue. Moreover, it reduced morphological and pathological changes found in the lungs, including neutrophil infiltration, edema and alveolar thickening. The present study concluded that Hev b 13 exerts anti-inflammatory effects and attenuates lung lesions in septal rats, showing potential for clinical application.

scholarly journals MEF2C alleviates acute lung injury in cecal ligation and puncture (CLP)-induced sepsis rats by up-regulating AQP1

2021 ◽  
Vol 49 (5) ◽  
pp. 117-124
Author(s):  
Wenmei Liang ◽  
Li Guo ◽  
Tonghua Liu ◽  
Song Qin
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Cecal Ligation ◽  
Weight Ratio ◽  
Dry Weight ◽  
Tunel Staining ◽  
Cecal Ligation And Puncture ◽  
Tnf Α ◽  
Factor Α

Background: Sepsis is a systemic inflammatory response syndrome and leads to patient’s death. Objective: To investigate the effect of myocyte enhancer factor 2 (MEF2C) on acute lung injury (ALI) with sepsis and its possible mechanism.Material and Methods: The cecal ligation and puncture (CLP)-induced sepsis rat model was established. The lung injury was determined by lung wet–dry weight ratio, the concentration of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), Interlukin (IL)-6, IL-1β, and IL-10, were measured by the enzyme-linked-immunosorbent serologic assay kit. The cell apoptosis was detected by TUNEL staining assay.Results: Interestingly, MEF2C was down-regulated in this model. Moreover, adeno-associated virus (AAV)-MEF2C treatment markedly suppressed TNF-α, IL-1β, and IL-6 concentrations but promoted IL-10 concentration in serum in CLP-challenged rats. Besides, overexpression of MEF2C alleviates CLP-induced lung injury. Interestingly, AAV-MEF2C treatment was confirmed to suppress apoptosis in CLP-induced sepsis rats as well as promote aquaporin APQ1 expres-sion. Mechanistically, the rescue experiments indicated that MEF2C alleviated CLP-induced lung inflammatory response and apoptosis via up-regulating AQP1.Conclusion: In summary, overexpression of MEF2C suppressed CLP-induced lung inflamma-tory response and apoptosis via up-regulating AQP1, providing a novel therapeutic target for sepsis-induced ALI.

scholarly journals Oroxylin A alleviates immunoparalysis of CLP mice by degrading CHOP through interacting with FBXO15

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Zhaoxin Zhang ◽  
Yun Wang ◽  
Yating Shan ◽  
Ri Zhou ◽  
Wu Yin
Keyword(s):  
Inflammatory Response ◽  
Cecal Ligation ◽  
Inflammatory Factors ◽  
Cecal Ligation And Puncture ◽  
Oroxylin A ◽  
Clinical Sepsis ◽  
Homologous Protein ◽  
Proteasome Pathway ◽  
Late Stages ◽  
H 30

Abstract Clinical reports have found that with the improvement of treatment, most septic patients are able to survive the severe systemic inflammatory response and to enter the immunoparalysis stage. Considering that immunoparalysis leads to numerous deaths of clinical sepsis patients, alleviation of the occurrence and development of immunoparalysis has become a top priority in the treatment of sepsis. In our study, we investigate the effects of oroxylin A on sepsis in cecal ligation and puncture (CLP) mice. We find that the 60 h + 84 h (30 mg/kg) injection scheme of oroxylin A induce the production of pro-inflammatory factors, and further significantly improves the survival of CLP mice during the middle or late stages of sepsis. Mechanistically, C/EBP-homologous protein (CHOP) is upregulated and plays anti-inflammatory roles to facilitate the development of immunoparalysis in CLP mice. Oroxylin A induces the transcription of E3 ligase F-box only protein 15 gene (fbxo15), and activated FBXO15 protein binds to CHOP and further mediates the degradation of CHOP through the proteasome pathway, which eventually relieves the immunoparalysis of CLP mice. Taken together, these findings suggest oroxylin A relieves the immunoparalysis of CLP mice by degrading CHOP through interacting with FBXO15.

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