scholarly journals Anti-Septic Potential of 7-α-Obacunyl Acetate Isolated from the Toona sinensis on Cecal Ligation/Puncture Mice via Suppression of JAK-STAT/NF-κB Signal Pathway

2021 ◽  
Vol Volume 14 ◽  
pp. 1813-1821
Author(s):  
Duo Li ◽  
Yibing Weng ◽  
Guan Wang ◽  
Genshen Zhen
Keyword(s):  
Cecal Ligation ◽  
Signal Pathway ◽  
Toona Sinensis ◽  
Cecal Ligation Puncture

scholarly journals Retracted: Inhibition of MicroRNA-23b Attenuates Immunosuppression During Late Sepsis Through NIK, TRAF1, and XIAP

2018 ◽  
Vol 218 (2) ◽  
pp. 300-311 ◽  
Author(s):  
Haiju Zhang ◽  
Hui Li ◽  
Aamir Shaikh ◽  
Yi Caudle ◽  
Baozhen Yao ◽  
...  
Keyword(s):  
T Cell ◽  
Cecal Ligation ◽  
Nuclear Factor Κb ◽  
Interleukin 10 ◽  
Signal Pathway ◽  
Interleukin 4 ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Luciferase Reporter ◽  
Apoptosis Protein ◽  
Cecal Ligation Puncture

AbstractBackgroundmicroRNA-23b (miR-23b) is a multiple functional miRNA. We hypothesize that miR-23b plays a role in the pathogenesis of sepsis. Our study investigated the effect of miR-23b on sepsis-induced immunosuppression.MethodsMice were treated with miR-23b inhibitors by tail vein injection 2 days after cecal ligation puncture (CLP)–induced sepsis. Apoptosis in spleens and apoptotic signals were investigated, and survival was monitored. T-cell immunoreactivities were examined during late sepsis. Nuclear factor κB (NF-κB)–inducing kinase (NIK), tumor necrosis factor (TNF)–receptor associated factor 1 (TRAF1), and X-linked inhibitor of apoptosis protein (XIAP), the putative targets of miR-23b, were identified by a dual-luciferase reporter assay.ResultsmiR-23b expression is upregulated and sustained during sepsis. The activation of the TLR4/TLR9/p38 MAPK/STAT3 signal pathway contributes to the production of miR-23b in CLP-induced sepsis. miR-23b inhibitor decreased the number of spleen cells positive by terminal deoxynucleotidyl transferase dUTP nick-end labeling and improved survival. miR-23b inhibitor restored the immunoreactivity by alleviating the development of T-cell exhaustion and producing smaller amounts of immunosuppressive interleukin 10 and interleukin 4 during late sepsis. We demonstrated that miR-23b mediated immunosuppression during late sepsis by inhibiting the noncanonical NF-κB signal and promoting the proapoptotic signal pathway by targeting NIK, TRAF1, and XIAP.ConclusionsInhibition of miR-23b reduces late-sepsis-induced immunosuppression and improves survival. miR-23b might be a target for immunosuppression.

EFFECTS OF TYRPHOSTIN AG-556 ON RAT SHOCK INDUCED BY CECAL LIGATION PUNCTURE OR LPS.

Shock ◽  
1998 ◽  
Vol 9 (Supplement) ◽  
pp. 33
Author(s):  
S. Ogura ◽  
O. Umegaki ◽  
I. B. Cochran ◽  
P. V. Halushka ◽  
J. A. Cook
Keyword(s):  
Cecal Ligation ◽  
Cecal Ligation Puncture

LEUKOCYTE-ENDOTHELIUM INTERACTIONS AFTER HEMORRHAGIC SHOCK/REPERFUSION AND CECAL LIGATION/PUNCTURE

Shock ◽  
2006 ◽  
Vol 26 (2) ◽  
pp. 180-186 ◽  
Author(s):  
Naomi Kondo Nakagawa ◽  
Rafael Aydar Nogueira ◽  
Cristiano Jesus Correia ◽  
S??lvia Regina Shiwa ◽  
Jos?? W??lber Miranda Costa Cruz ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Cecal Ligation ◽  
Cecal Ligation Puncture

scholarly journals Melatonin Alleviates Renal Injury in Mouse Model of Sepsis

2021 ◽  
Vol 12 ◽  
Author(s):  
Liyang Chen ◽  
Zhijian Han ◽  
Zhiguang Shi ◽  
Chao Liu ◽  
Qiulun Lu
Keyword(s):  
Renal Injury ◽  
Oxidant Stress ◽  
Mrna Level ◽  
Cecal Ligation ◽  
Kidney Injury ◽  
Protective Role ◽  
Cecal Ligation Puncture ◽  
Species Production

Melatonin (N-acetyl-5-methoxytryptamine; MLT) has been shown to have a renal-protective effect against kidney injury. However, the mechanisms underlying the protective role of MLT in sepsis-induced renal injury are yet to be revealed. In this study, MLT alleviated renal dysfunction with the increase of BUN (blood urea nitrogen) and SCR (serum creatinine) and reduction of fibrosis in the CLP (cecal ligation puncture) model. RNA-seq analysis showed that MLT repressed the oxidant stress in response to kidney injury. Our in vitro study showed that MLT suppresses LPS-induced accumulation of ROS (reactive oxygen species) production via SOD2 downregulation and Nox4 upregulation in HK-2 cells. Furthermore, we found that MLT alleviated the inflammatory response, with the mRNA-level reduction of Il-1α, Il-1β, Mcp-1, and Tgf-β1. Taken together, in evaluating the therapeutic effect of MLT on sepsis-induced acute kidney injury, the results showed that MLT alleviated renal damage by regulating the production of ROS.

scholarly journals Trigonoside II mitigates sepsis-induced myocardial injury via reduction in oxidative stress and regulation of TLR- 4/NF-kB inflammatory pathway

2020 ◽  
Vol 19 (6) ◽  
pp. 1161-1166
Author(s):  
Fengru Wang ◽  
Lili Wu ◽  
Qun Liang
Keyword(s):  
Oxidative Stress ◽  
Myocardial Injury ◽  
Caspase 3 ◽  
Cecal Ligation ◽  
Rat Serum ◽  
Inflammatory Pathway ◽  
Post Surgery ◽  
Tnf Α ◽  
Protein Expressions ◽  
Cecal Ligation Puncture

Purpose: To investigate the protective effect of trigonoside II against sepsis-induced myocardial injury in rats, and the mechanism involved. Methods: Adult male Sprague Dawley rats (n = 30) weighing 200 - 230 g (mean weight = 215 ± 15 g) were used for this study. The rats were randomly assigned to 3 groups (10 rats/group): sham, cecal ligation puncture (CLP), and trigonoside II. Rats in the treatment group received trigonoside II at a dose of 2 mg/kg intraperitoneally (i.p.) at 3, 12 and 24 h post-surgery. Sepsis was induced using CLP method. Lactate  dehydrogenase (LDH) and creatine kinase (CK-MB) activities, and hemodynamic functions were determined in the rats. The levels of interleukin (IL)-1β and IL-6, and tumor necrosis factor α (TNF-α) were assayed in rat serum. Oxidative stress and myocardial cell apoptosis were determined by measuring malondialdehyde (MDA) levels, while activities of glutathione peroxidase (GPx), superoxide dismutase (SOD) and myeloperoxidase (MPO), as well as levels of expression of bax, bcl-2 and caspase-3 were also assessed. Results: Treatment of myocardial injury rats with trigonoside II led to significant reductions in the activities of LDH, CK-MB and MPO, and decreases in levels of IL-1β, IL-6 and TNF-α (p < 0.05). It also significantly reversed the effects of sepsis on rat hemodynamic functions (p < 0.05). Trigonoside IItreatment significantly reduced MDA levels in rat myocardial tissues, but significantly increased SOD and GPx activities (p < 0.05). It significantly down-regulated protein expressions of NF-kB and TLR-4 in myocardial tissues (p < 0.05). The number of apoptotic cells and activity of caspase-3 were significant increased in myocardial tissues of rats in CLP group, when compared with sham group, but were reduced significantly in myocardial tissues of trigonoside II-treated rats (p < 0.05). Similarly, trigonoside II treatment down-regulated the protein expressions of caspase-3 and bax, but upregulated bcl-2 protein expression in the rat myocardial tissues (p < 0.05). Conclusion: The results of this study indicate that trigonoside II confers protection on sepsis-induced myocardial injury via reduction in oxidative stress and regulation of TLR-4/NF-kB inflammatory pathway. Keywords: Cecal ligation puncture, Myocardial injury, Oxidative stress, Sepsis, Trigonoside II

scholarly journals In vivo observation of mesenteric leukocyte-endothelial interactions after cecal ligation/puncture and surgical sepsis source control

Clinics ◽  
2007 ◽  
Vol 62 (3) ◽  
pp. 321-326 ◽  
Author(s):  
Naomi K. Nakagawa ◽  
José Jukemura ◽  
Priscila Aikawa ◽  
Rafael A. Nogueira ◽  
Luiz F. Poli-de-Figueiredo ◽  
...  
Keyword(s):  
Cecal Ligation ◽  
Source Control ◽  
Cecal Ligation Puncture

HEART PROTEIN SYNTHESIS AFTER CECAL LIGATION & PUNCTURE (CLP) IN THE RAT

Shock ◽  
1999 ◽  
Vol 11 (Supplement) ◽  
pp. 12 ◽  
Author(s):  
M. OʼLeary ◽  
C. Ferguson ◽  
C. Hinds ◽  
J. Coakley ◽  
V. Preedy
Keyword(s):  
Protein Synthesis ◽  
Cecal Ligation ◽  
Cecal Ligation Puncture

scholarly journals Vascular endothelial growth factor is an important determinant of sepsis morbidity and mortality

2006 ◽  
Vol 203 (6) ◽  
pp. 1447-1458 ◽  
Author(s):  
Kiichiro Yano ◽  
Patricia C. Liaw ◽  
Janet M. Mullington ◽  
Shu-Ching Shih ◽  
Hitomi Okada ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cecal Ligation ◽  
Morbidity And Mortality ◽  
Vascular Endothelial ◽  
Cardiac Physiology ◽  
Pathophysiological Role ◽  
Cecal Ligation Puncture ◽  
Endothelial Growth Factor ◽  
Circulating Levels

Sepsis, the systemic inflammatory response to infection, is a leading cause of morbidity and mortality. The mechanisms of sepsis pathophysiology remain obscure but are likely to involve a complex interplay between mediators of the inflammatory and coagulation pathways. An improved understanding of these mechanisms should provide an important foundation for developing novel therapies. In this study, we show that sepsis is associated with a time-dependent increase in circulating levels of vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) in animal and human models of sepsis. Adenovirus-mediated overexpression of soluble Flt-1 (sFlt-1) in a mouse model of endotoxemia attenuated the rise in VEGF and PlGF levels and blocked the effect of endotoxemia on cardiac function, vascular permeability, and mortality. Similarly, in a cecal ligation puncture (CLP) model, adenovirus–sFlt-1 protected against cardiac dysfunction and mortality. When administered in a therapeutic regimen beginning 1 h after the onset of endotoxemia or CLP, sFlt peptide resulted in marked improvement in cardiac physiology and survival. Systemic administration of antibodies against the transmembrane receptor Flk-1 but not Flt-1 protected against sepsis mortality. Adenovirus-mediated overexpression of VEGF but not PlGF exacerbated the lipopolysaccharide-mediated toxic effects. Together, these data support a pathophysiological role for VEGF in mediating the sepsis phenotype.

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