cecal ligation and puncture
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2022 ◽  
Vol 8 (1) ◽  
pp. 1-8
Author(s):  
Derya Güzel ERDOĞAN ◽  
Ayhan TANYELİ ◽  
Fazile Nur EKİNCİ AKDEMİR ◽  
Mustafa Can GÜLER ◽  
Ersen ERASLAN ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Luorui Shang ◽  
Yuhan Liu ◽  
Jinxiao Li ◽  
Guangtao Pan ◽  
Fangyuan Zhou ◽  
...  

Aims: Emodin is an anthraquinone extracted from Polygonum multiflorum, which has potential anti-inflammatory and anti-oxidative stress effects. However, the possible protective mechanism of emodin is unclear. The purpose of this study was to investigate the protective mechanism of emodin against cecal ligation and puncture and LPS-induced intestinal mucosal barrier injury through the VDR/ Nrf2 /HO-1 signaling pathway.Methods: We established a mouse model of sepsis by cecal ligation and puncture (CLP), and stimulated normal intestinal epithelial cells with lipopolysaccharide (LPS). VDR in cellswas down-regulated by small interfering ribonucleic acid (siRNA) technology.Mice were perfused with VDR antagonists ZK168281 to reduce VDR expression and mRNA and protein levels of VDR and downstream molecules were detected in cells and tissue. Inflammation markers (tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6)) and oxidative stress markers (superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione (GSH)) were measured in serum and intestinal tissueby enzym-linked immunosorbent assay. The expression of VDR in intestinal tissue was detected by immunofluorescence. Histopathological changes were assessed by hematoxylin and eosin staining.Results: In NCM460 cells and animal models, emodin increased mRNA and protein expression of VDR and its downstream molecules. In addition, emodin could inhibit the expressions of TNF-α, IL-6 and MDA in serum and tissue, and increase the levels of SOD and GSH. The protective effect of emodin was confirmed in NCM460 cells and mice, where VDR was suppressed. In addition, emodin could alleviate the histopathological damage of intestinal mucosal barrier caused by cecal ligation and puncture.Conclusion: Emodin has a good protective effect against sepsis related intestinal mucosal barrier injury, possibly through the VDR/ Nrf2 /HO-1 pathway.


2021 ◽  
Vol 147 (4) ◽  
pp. 358-366
Author(s):  
Amira M. Aboyoussef ◽  
Mostafa Kamal Mohammad ◽  
Ali Ahmed Abo-Saif ◽  
Basim A.S. Messiha

Drug Research ◽  
2021 ◽  
Author(s):  
Hasan Yousefi-Manesh ◽  
Samira Shirooie ◽  
Tayebeh Noori ◽  
Seyed Mohammad Tavangar ◽  
Mohammad Sheibani ◽  
...  

AbstractSepsis is a severe systemic inflammatory response with high mortality rate resulting from different microorganisms. Cytokines activation is essential for the immune response, but in painful conditions like sepsis, cytokines act as a double-edged sword and dysregulate immune response which is life-threatening owing to multiple organ dysfunction. The abnormality in 5-HT function is involved in pathological conditions like irritable bowel syndrome, inflammation, myocardial ischemia, itch and renal injury. Sumatriptan, a 5-HT1B/1D agonist, has anti-inflammatory and anti-oxidative stress effects on animal models. This study was aimed to assess the effects of sumatriptan on kidney injury, the levels of pro-inflammatory cytokines and the percentage of survival in (CLP)-induced sepsis were examined.Cecal ligation and puncture (CLP) model was done on adult C57BL/6 male mice to induce Polymicrobial sepsis. Sumatriptan was injected intraperitoneally 1 h after the sepsis induction by CLP at doses of 0.1, 0.3, and 1 mg/kg in 3 treatment groups. To study the effect of sumatriptan on short-term survival, septic animals were detected 72 h after CLP. Serum levels of TNF-α, IL-1β, IL-6 and IL-10 were evaluated. To study sepsis-induced acute renal failure, kidney functional biomarkers and histopathological alterations were evaluated.Sumatriptan (0.3 mg/kg) administration significantly enhanced survival rate (P<0.01) compared to the CLP group. The beneficial effects of sumatriptan were related to a significant decrease in the pro-inflammatory cytokines and elevated level of IL-10. Sumatriptan presented protective effects on kidney biomarkers and histopathology assay.Anti-inflammatory effects of sumatriptan lead to decrease mortality rate and inflammatory cytokines in CLP induction sepsis in C57BL/6 mice.


2021 ◽  
Author(s):  
Keita Ikeda ◽  
Hari Prasad Osuru ◽  
Robert H. Thiele

Abstract BACKGROUNDSeveral studies have also shown that short-term exposure to volatile anesthetic agents (VAA) affects proinflammatory pathways such as the cytokine response and provides a protective effect that improves the outcome of sepsis. In contrast, Propofol has been shown to have no protective effect on sepsis in murine and rat models and may increase morbidity and mortality. This study aimed to investigate the efficacy of longer-term exposure to anesthetics, isoflurane, and Propofol (72 hours).METHODSAnimals were randomized into four groups: Isoflurane during surgery followed by three days of 0.8% isoflurane (and Intralipid IV), Propofol during surgery and 314 ug/kg/hr Propofol for three days, isoflurane during surgery and Intralipid for three days, and Propofol during surgery and Intralipid for three days.After induction via Propofol or isoflurane, animals spontaneously ventilated via nose cone with 100% oxygen. Propofol or Intralipid was administered through a 22 gauge intravenous catheter inserted into the jugular vein. Sepsis was induced in the rats by performing cecal ligation and puncture (CLP) through a paramedian incision into the abdominal cavity. The surgical concentration of isoflurane was kept at 2%, Propofol was maintained at 800 ug/kg/hr maintenance. After the recovery and three days of exposure to Intralipid or anesthetic agents, the rats were allowed to roam free in an adequately vented, temperature and humidity-controlled cage with food and water ad libitum. Survival data were summarized using the Kaplan-Meier curve with Log-Rank test to determine significance.RESULTSLog-Rank test for postoperative anesthetic agent groups showed that rats that received isoflurane for three days survived longer than the 72-hour postoperative Propofol group (P = 0.0002). Within the postoperative, no anesthetic agent (control) group, the group that received isoflurane during surgery survived longer than the Propofol during surgery group (P = 0.0081). Within the postoperative Intralipid groups, the male rats did not perform well with Propofol against isoflurane (P = 0.2599).CONCLUSIONSExposure of rats to isoflurane may prolong survival in CLP as compared to exposure to Propofol. This was true for rats with limited exposure during surgery with no postoperative anesthetics and those receiving intraoperative isoflurane with postoperative isoflurane.


Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1676
Author(s):  
Aron B. Fisher ◽  
Chandra Dodia ◽  
Jian-Qin Tao ◽  
Sheldon I. Feinstein ◽  
Shampa Chatterjee

The use of agents to inhibit the production of reactive oxygen species (ROS) has been proposed for the treatment of Acute Lung Injury (ALI). However, this approach also inhibits the bactericidal activity of polymorphonuclear leucocytes (PMN) and other cells, raising the possibility of aggravating lung injury in ALI associated with bacterial infection. We used the cecal ligation and puncture (CLP) model of ALI associated with sepsis to investigate the effect of inhibiting NADPH oxidase 2 (NOX2)-derived ROS production, the main source of ROS in lungs. A phospholipase A2 inhibitor called peroxiredoxin 6 inhibitory peptide-2 (PIP-2) was used to inhibit NOX2 activation; the peptide prevents liberation of Rac, a necessary NOX2 co-factor. At 18 h after intravenous treatment with 2 µg PIP-2 /gram body weight (wt), the number of colony-forming bacteria in lungs and peritoneal fluid of mice with CLP was approximately doubled as compared to untreated mice. Treatment with 10 µg PIP-2/g body wt resulted in 100% mortality within 18 hr. Antibiotic treatment abolished both the increase in lung bacteria with low dose PIP-2 and the increased mortality with high dose PIP-2. Treatment with PIP-2 plus antibiotics resulted in significantly improved lung histology, decreased PMN infiltration, decreased lung fluid accumulation, and decreased oxidative lung injury compared to antibiotics alone. We conclude that the administration of PIP-2 provides partial protection against lung injury in a model of ALI due to bacterial infection, while concurrent antibiotic treatment abolishes the deleterious effects of PIP-2 on lung bacterial clearance. These results suggest that addition of PIP-2 to the antibiotic regimen is beneficial for treatment of ALI associated with bacterial infection.


Life Sciences ◽  
2021 ◽  
pp. 120033
Author(s):  
Raquel Pires Nakama ◽  
Aparecida Donizette Malvezi ◽  
Maria Isabel Lovo-Martins ◽  
Lucas Felipe dos Santos ◽  
Ana Paula Canizares Cardoso ◽  
...  

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