scholarly journals A New Approach to Monitoring and Evaluation of Cecal Ligation and Puncture Sepsis Model

2021 ◽  
Vol 3 (2) ◽  
pp. 97-106
Author(s):  
Arezou Khosrojerdi ◽  
◽  
Sara Soudi ◽  
Ahmad Zavaran Hosseini ◽  
Seyed Mahmoud Hashemi ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Clinical Chemistry ◽  
Cecal Ligation ◽  
Serum Levels ◽  
Cecal Ligation And Puncture ◽  
Inflammatory Status ◽  
Sepsis Model ◽  
Tnf Α ◽  
Systemic Inflammatory Disease ◽  
Tgf Β1

Background: Sepsis is a systemic inflammatory disease in response to the pathogens that leads to vital organ failures the failure of vital organs. Appropriate animal models should be developed to measure the effectiveness of therapeutic methods. Cecal Ligation and Puncture (CLP) is the most widely used methods of creating the sepsis model. Some variables interfere in the creation of the CLP model which terminated to result in an unrepeatable dynamic of the inflammatory responses. The current research, suggests presents the simultaneous study of inflammatory responses in serum and liver as a criterion for determining the inflammatory status of the CLP model. Materials and Methods: CLP model was induced in 15 female C57bl/6 mice. IL-6, TNF-α, IL-10, and TGF-β1 cytokines levels were measured at 24, 48, and 72 hours after CLP induction in both serum and liver tissue by ELISA method. Serum levels of liver enzymes were analyzed by the clinical chemistry analyzer. All studies were performed in healthy mice as well. The results were reported as Mean±SD. Results: The levels of IL-10 and TGF- β1 in the liver is were significantly (P≤0.05) higher than serum. The production of IL-10 and TGF- β1 in the serum and liver reaches its maximum at peaked 24 and 72 hours after CLP induction. The level of TNF-α in the liver is was significantly (P≤0.05) higher than serum with a maximum production 24 hours after CLP induction. Conclusion: Serum is not a good representative of the inflammatory condition in sepsis. Therefore, it is suggested that local inflammatory responses be considered in evaluating the model, and the determination of drug efficacy.

scholarly journals Senkyunolide I Protects against Sepsis-Associated Encephalopathy by Attenuating Sleep Deprivation in a Murine Model of Cecal Ligation and Puncture

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Jian Xie ◽  
Zhen-zhen Zhao ◽  
Peng Li ◽  
Cheng-long Zhu ◽  
Yu Guo ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Cognitive Dysfunction ◽  
Murine Model ◽  
Inflammatory Responses ◽  
Cecal Ligation ◽  
Signaling Proteins ◽  
Cecal Ligation And Puncture ◽  
Inflammatory Signaling ◽  
Tnf Α ◽  
Senkyunolide I

Sepsis may lead to sleep deprivation, which will promote the development of neuroinflammation and mediate the progression of sepsis-associated encephalopathy (SAE). Senkyunolide I, an active component derived from an herb medicine, has been shown to provide a sedative effect to improve sleep. However, its role in sepsis is unclear. The present study was performed to investigate whether Senkyunolide I protected against SAE in a murine model of cecal ligation and puncture (CLP). Here, we showed that Senkyunolide I treatment improved the 7-day survival rate and reduced the excessive release of cytokines including TNF-α, IL-6, and IL-1β. A fear conditioning test was performed, and the results showed that Senkyunolide I attenuated CLP-induced cognitive dysfunction. Senkyunolide I treatment also decreased the phosphorylation levels of inflammatory signaling proteins, including p-ERK, p-JNK, p-P38, and p-P65, and the level of inflammatory cytokines, including TNF-α, IL-6, and IL-1β, in the hippocampus homogenate. Sleep deprivation was attenuated by Senkyunolide I administration, as demonstrated by the modification of the BDNF and c-FOS expression. When sleep deprivation was induced manually, the protective effect of Senkyunolide I against inflammatory responses and cognitive dysfunction was reversed. Our data demonstrated that Senkyunolide I could protect against sepsis-associated encephalopathy in a murine model of sepsis via relieving sleep deprivation.

scholarly journals Senkyunolide I Protects Against Sepsis-associated Encephalopathy by Attenuating Sleep Deprivation in a Murine Model of Cecal Ligation and Puncture

2020 ◽  
Author(s):  
Jian Xie ◽  
Zhen-zhen Zhao ◽  
Peng Li ◽  
Cheng-long Zhu ◽  
Yu Guo ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Cognitive Dysfunction ◽  
Murine Model ◽  
Inflammatory Responses ◽  
Cecal Ligation ◽  
Tunel Staining ◽  
Cecal Ligation And Puncture ◽  
Inflammatory Signaling ◽  
Tnf Α ◽  
Senkyunolide I

Abstract Background: Sepsis may lead to sleep deprivation, which will promote the development of neuroinflammation and mediate the progression of sepsis associated encephalopathy (SAE). Senkyunolide I, an active component derived from an herb medicine, has been shown to provide sedative effect to improve sleep. But its role in sepsis is unclear. The present study was performed to investigate whether Senkyunolide I protected against SAE in a murine model of cecal ligation and puncture (CLP).Methods: The male C57BL/6 mice were used to investigate the effects of Senkyunolide I on SAE. The related protein of the sleep deprivation and inflammatory signaling pathway was detected by western blot. The activation of microglia and the neuronal apoptosis were separately detected by immunofluorescence staining and TUNEL staining.Results: Here, we showed that Senkyunolide I treatment improved the 7-day survival rate and reduced the excessive release of cytokines including TNF-α, IL-6 and IL-1β. A fear conditioning test was performed and the result showed that Senkyunolide I attenuated CLP-induced cognitive dysfunction. Senkyunolide I treatment also decreased the phosphorylation levels of inflammatory signaling proteins, including p-ERK, p-JNK, p-P38, p-P65, and the level of inflammatory cytokines, including TNF-α, IL-6 and IL-1β, in the hippocampus homogenate. The sleep deprivation was attenuated by Senkyunolide I administration, as demonstrated by the modification of the BDNF and c-FOS expression. When sleep deprivation was induced manually, the protective effect of Senkyunolide I against inflammatory responses and cognitive dysfunction was reversed. Conclusion: Our data demonstrated that Senkyunolide I could protect against sepsis-associated encephalopathy in a murine model of sepsis via relieving sleep deprivation.

scholarly journals In Vitro Evaluation of the Anti-Inflammatory Effect of KMUP-1 and in Vivo Analysis of Its Therapeutic Potential in Osteoarthritis

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 615
Author(s):  
Shang-En Huang ◽  
Erna Sulistyowati ◽  
Yu-Ying Chao ◽  
Bin-Nan Wu ◽  
Zen-Kong Dai ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Antioxidant Properties ◽  
Serum Levels ◽  
Gene Expressions ◽  
Tnf Α ◽  
Anti Inflammatory

Osteoarthritis is a degenerative arthropathy that is mainly characterized by dysregulation of inflammatory responses. KMUP-1, a derived chemical synthetic of xanthine, has been shown to have anti-inflammatory and antioxidant properties. Here, we aimed to investigate the in vitro anti-inflammatory and in vivo anti-osteoarthritis effects of KMUP-1. Protein and gene expressions of inflammation markers were determined by ELISA, Western blotting and microarray, respectively. RAW264.7 mouse macrophages were cultured and pretreated with KMUP-1 (1, 5, 10 μM). The productions of TNF-α, IL-6, MMP-2 and MMP- 9 were reduced by KMUP-1 pretreatment in LPS-induced inflammation of RAW264.7 cells. The expressions of iNOS, TNF-α, COX-2, MMP-2 and MMP-9 were also inhibited by KMUP-1 pretreatment. The gene expression levels of TNF and COX families were also downregulated. In addition, KMUP-1 suppressed the activations of ERK, JNK and p38 as well as phosphorylation of IκBα/NF-κB signaling pathways. Furthermore, SIRT1 inhibitor attenuated the inhibitory effect of KMUP-1 in LPS-induced NF-κB activation. In vivo study showed that KMUP-1 reduced mechanical hyperalgesia in monoiodoacetic acid (MIA)-induced rats OA. Additionally, KMUP-1 pretreatment reduced the serum levels of TNF-α and IL-6 in MIA-injected rats. Moreover, macroscopic and histological observation showed that KMUP-1 reduced articular cartilage erosion in rats. Our results demonstrated that KMUP-1 inhibited the inflammatory responses and restored SIRT1 in vitro, alleviated joint-related pain and cartilage destruction in vivo. Taken together, KMUP-1 has the potential to improve MIA-induced articular cartilage degradation by inhibiting the levels and expression of inflammatory mediators suggesting that KMUP-1 might be a potential therapeutic agent for OA.

scholarly journals Triglyceride-rich lipoproteins prevent septic death in rats.

1995 ◽  
Vol 182 (1) ◽  
pp. 267-272 ◽  
Author(s):  
T E Read ◽  
C Grunfeld ◽  
Z L Kumwenda ◽  
M C Calhoun ◽  
J P Kane ◽  
...  
Keyword(s):  
Lipid Emulsion ◽  
Tumor Necrosis ◽  
Lethal Dose ◽  
Cecal Ligation ◽  
Serum Levels ◽  
Cecal Ligation And Puncture ◽  
Gram Negative ◽  
Necrosis Factor ◽  
Serum Tumor Necrosis

Triglyceride-rich lipoproteins bind and inactive bacterial endotoxin in vitro and prevent death when given before a lethal dose of endotoxin in animals. However, lipoproteins have not yet been demonstrated to improve survival in polymicrobial gram-negative sepsis. We therefore tested the ability of triglyceride-rich lipoproteins to prevent death after cecal ligation and puncture (CLP) in rats. Animals were given bolus infusions of either chylomicrons (1 g triglyceride/kg per 4 h) or an equal volume of saline for 28 h after CLP. Chylomicron infusions significantly improved survival (measured at 96 h) compared with saline controls (80 vs 27%, P < or = 0.03). Chylomicron infusions also reduced serum levels of endotoxin, measured 90 min (26 +/- 3 vs 136 +/- 51 pg/ml, mean +/- SEM, P < or = 0.03) and 6 h (121 +/- 54 vs 1,026 +/- 459 pg/ml, P < or = 0.05) after CLP. The reduction in serum endotoxin correlated with a reduction in serum tumor necrosis factor, measured 6 h after CLP (0 +/- 0 vs 58 +/- 24 pg/ml, P < or = 0.03), suggesting that chylomicrons improve survival in this model by limiting macrophage exposure to endotoxin and thereby reducing secretion of inflammatory cytokines. Infusions of a synthetic triglyceride-rich lipid emulsion (Intralipid; KabiVitrum, Inc., Alameda, CA) (1 g triglyceride/kg) also significantly improved survival compared with saline controls (71 vs 27%, P < or = 0.03). These data demonstrate that triglyceride-rich lipoproteins can protect animals from lethal polymicrobial gram-negative sepsis.

l-Carnitine-induced amelioration of HFD-induced hepatic dysfunction is accompanied by a reduction in hepatic TNF-α and TGF-β1

2018 ◽  
Vol 96 (6) ◽  
pp. 713-725 ◽  
Author(s):  
Mabrouk Attia Abd Eldaim ◽  
Fatma Mohamed Ibrahim ◽  
Saher Hassan Orabi ◽  
Azza Hassan ◽  
Hesham Saad El Sabagh
Keyword(s):  
Protein Expression ◽  
High Density Lipoprotein ◽  
Body Mass ◽  
Density Lipoprotein ◽  
Basal Diet ◽  
Serum Levels ◽  
High Density ◽  
Control Group ◽  
Tnf Α ◽  
Tgf Β1

In this study, we evaluated the possible mechanisms through which l-carnitine ameliorates the adverse effects from obesity in rats, induced with a high-fat diet (HFD). For this, 56 albino Wister rats were randomly assigned to 7 groups. The control group was fed a basal diet and injected with saline. The second group was fed the basal diet and injected with l-carnitine (200 mg/kg body mass, by intraperitoneal injection; i.p.). The third group were fed the HFD. The fourth group was fed the HFD and injected with l-carnitine (200 mg/kg body mass, i.p.) for 8 weeks. The fifth group was fed the HFD for 10 weeks. The sixth group were fed the HFD for 10 weeks and were also injected with l-carnitine (200 mg/kg body mass, i.p.) during the final 2 weeks. The seventh group was fed the HFD diet for 8 weeks then the basal diet for 2 weeks. The HFD induced significantly increased levels of hyperglycemia, lipid peroxidation, pathological changes, TNF-α and TGF-β1 protein expression in hepatic tissue, food intake, body weight gain, serum levels of total and non-high-density lipoprotein cholesterol, ketone bodies, triacylglycerol, urea, creatinine, AST, and ALT. However, the HFD diet significantly decreased serum levels of high-density lipoprotein (HDL) and hepatic levels of reduced glutathione. l-Carnitine ameliorated the effects of the HFD on the above-mentioned parameters. This study indicated that l-carnitine had protective and curative effects against HFD-induced hepatosteatosis by reducing hepatic oxidative stress and protein expression of TNF-α and TGF-β1.

The Possible Protective Effect of Selenium on Liver Dysfunction in a Rat Model of Extrahepatic Cholestasis

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Fatma M Lebda ◽  
Sahar M El Agaty ◽  
Noha A Nassef ◽  
Marina A Aziz
Keyword(s):  
Bile Duct ◽  
Transforming Growth Factor ◽  
Group Versus ◽  
Serum Levels ◽  
Selenium Supplementation ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Tgf Β1 ◽  
Necrosis Factor

Abstract Background Oxidative stress and inflammation are primarily implicated in the development and progression of liver injury during cholestasis. Selenium, a known essential antioxidant trace element, was found to provide a remarkable antioxidant and anti-inflammatory effects on various diseases. Aim This study was planned to evaluate the possible protective effect of selenium supplementation in a rat model of chronic cholestasis. Design Experimental study. Methods This study was carried out on adult male rats allocated randomly into sham, bile duct ligated (BDL), and BDL-selenium treated (BDL-Se) groups. Sodium selenite was given by gavage daily, in a dose of 100 µg/kg for 6 weeks, starting 2 weeks before the BDL. Results BDL group presented a significant increase in serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and liver levels of malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), and transforming growth factor beta 1(TGF-β1), associated with a significant decrease in serum levels of total proteins (TP) compared to sham group . Selenium supplementation significantly lowered serum levels of AST, ALT, ALP, and liver levels of MDA, TNF-α, and TGF-β1 along with a significant increase in serum TP in BDL-Se group versus BDL rats. Histological analysis of liver showed a significant attenuation of the inflammatory score and a significant decrease in the percentage area of collagen deposition in BDL-Se group versus BDL rats. Conclusion Selenium supplementation reduces liver injury and improves liver functions in experimental cholestasis probably by its antioxidant and anti-inflammatory activities, which further alleviate the liver fibrosis. Abbreviations BDL: bile duct ligated group, BDL-Se: bile duct ligated-selenium group, MDA: malondialdehyde, TNF-α: tumour necrosis factor-alpha, TGF-β1: transforming growth factor- beta1, ROS: reactive oxygen species, mRNA: messenger RNA, IL-6: interleukin-6, BW: body weight, AST: aspartate aminotransferase, ALT: alanine aminotransferase, ALP: alkaline phosphatase, TP: total proteins, CCl4: carbon tetrachloride, GPx: glutathione peroxidase enzyme, SOD: superoxide dismutase, IL-1: interleukin-1.

Anti-Inflammatory Effects of Exercise on Metabolic Syndrome Patients: A Systematic Review and Meta-Analysis

2020 ◽  
pp. 109980042095806 ◽  
Author(s):  
Heidar Alizaei Yousefabadi ◽  
Arghavan Niyazi ◽  
Sahar Alaee ◽  
Mehrdad Fathi ◽  
Gholam Rasul Mohammad Rahimi
Keyword(s):  
Metabolic Syndrome ◽  
Exercise Training ◽  
Inflammatory Markers ◽  
Meta Analysis ◽  
Serum Levels ◽  
Future Research ◽  
The Metabolic Syndrome ◽  
Inflammatory Status ◽  
Tnf Α ◽  
Training Impact

Background: Increments in inflammatory indicators and low levels of physical activity are correlated to the expansion of the metabolic syndrome (MetS). Objective: The purpose of this study was to establish if exercise training ameliorates inflammatory status in MetS patients. Data sources: PubMed, CINAHL, and Medline, Google Scholar, and Scopus databases and reference lists of included studies were searched. Study selection: Twenty randomized controlled trials (RCTs) of exercise-training impact on inflammatory markers (tumor necrosis factor (TNF) α, C-reactive protein (CRP), interleukin (IL) 6, IL-8, IL-10, and IL-18) with concurrent control groups were included in this analysis. Results: Results demonstrated an overall significant decrease in serum levels of TNF-α (mean difference (MD): −1.21 pg/ml; 95% confidence interval (CI): −1.77, −0.66), CRP (MD: −0.52 mg/l; 95% CI: −0.79, −0.25), IL-8 (MD: −1.31 pg/ml; 95% CI: −2.57, −0.06), and a significant increase in IL-10 (MD: 0.48 pg/ml; 95% CI: 0.10, 0.86). But exercise training did not change the level of IL-6 (MD: −0.69 pg/ml; 95% CI: −1.53, 0.14) and IL-18 (MD: −53.01 pg/ml; 95% CI: −166.64, 60.62). Conclusion: Exercise training improves TNF-α, CRP, IL-8, and IL-10 levels in patients with MetS. For some variables, isolated aerobic exercise, and combined aerobic and resistance exercise appears to be optimal. Future research is needed to clarify the mechanisms underlying exercise training’s effect on this population’s inflammatory markers. More studies are required to confirm these findings.

Alpha-lipoic acid as a potential target for the treatment of lung injury caused by cecal ligation and puncture-induced sepsis model in rats

Shock ◽  
2009 ◽  
pp. 1 ◽  
Author(s):  
Elif Cadirci ◽  
Berrin Zuhal Altunkaynak ◽  
Zekai Halici ◽  
Fehmi Odabasoglu ◽  
M. Hamidullah Uyanik ◽  
...  
Keyword(s):  
Lung Injury ◽  
Lipoic Acid ◽  
Cecal Ligation ◽  
Alpha Lipoic Acid ◽  
Cecal Ligation And Puncture ◽  
Potential Target ◽  
Sepsis Model
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