Atractylenolide III Ameliorates TNBS‐Induced Intestinal Inflammation in Mice by Reducing Oxidative Stress and Regulating Intestinal Flora

2021 ◽  
Author(s):  
Yan Ren ◽  
Wenwen Jiang ◽  
Chunli Luo ◽  
Xiaohan Zhang ◽  
Mingjin Huang
Keyword(s):  
Oxidative Stress ◽  
Intestinal Inflammation ◽  
Intestinal Flora ◽  
Atractylenolide Iii

scholarly journals A cafeteria diet triggers intestinal inflammation and oxidative stress in obese rats

2017 ◽  
Vol 117 (2) ◽  
pp. 218-229 ◽  
Author(s):  
K. Gil-Cardoso ◽  
I. Ginés ◽  
M. Pinent ◽  
A. Ardévol ◽  
X. Terra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intestinal Inflammation ◽  
Cafeteria Diet ◽  
Zucker Rats ◽  
Standard Diet ◽  
Metabolic Alterations ◽  
Genetic Obesity ◽  
Obesogenic Diet ◽  
The Impact ◽  
And Oxidative Stress

AbstractThe gastrointestinal alterations associated with the consumption of an obesogenic diet, such as inflammation, permeability impairment and oxidative stress, have been poorly explored in both diet-induced obesity (DIO) and genetic obesity. The aim of the present study was to examine the impact of an obesogenic diet on the gut health status of DIO rats in comparison with the Zucker (fa/fa) rat leptin receptor-deficient model of genetic obesity over time. For this purpose, female Wistar rats (n 48) were administered a standard or a cafeteria diet (CAF diet) for 12, 14·5 or 17 weeks and were compared with fa/fa Zucker rats fed a standard diet for 10 weeks. Morphometric variables, plasma biochemical parameters, myeloperoxidase (MPO) activity and reactive oxygen species (ROS) levels in the ileum were assessed, as well as the expressions of proinflammatory genes (TNF-α and inducible nitric oxide synthase (iNOS)) and intestinal permeability genes (zonula occludens-1, claudin-1 and occludin). Both the nutritional model and the genetic obesity model showed increased body weight and metabolic alterations at the final time point. An increase in intestinal ROS production and MPO activity was observed in the gastrointestinal tracts of rats fed a CAF diet but not in the genetic obesity model. TNF-α was overexpressed in the ileum of both CAF diet and fa/fa groups, and ileal inflammation was associated with the degree of obesity and metabolic alterations. Interestingly, the 17-week CAF group and the fa/fa rats exhibited alterations in the expressions of permeability genes. Relevantly, in the hyperlipidic refined sugar diet model of obesity, the responses to chronic energy overload led to time-dependent increases in gut inflammation and oxidative stress.

scholarly journals Atractylenolide III Attenuates Muscle Wasting in Chronic Kidney Disease via the Oxidative Stress-Mediated PI3K/AKT/mTOR Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Mingqing Wang ◽  
Rong Hu ◽  
Yanjing Wang ◽  
Lingyu Liu ◽  
Haiyan You ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Skeletal Muscles ◽  
Muscle Wasting ◽  
Mtor Pathway ◽  
C2c12 Myoblast ◽  
Model Group ◽  
Atractylenolide Iii

Oxidative stress contributes to muscle wasting in advanced chronic kidney disease (CKD) patients. Atractylenolide III (ATL-III), the major active constituent of Atractylodes rhizome, has been previously reported to function as an antioxidant. This study is aimed at investigating whether ATL-III has protective effects against CKD-induced muscle wasting by alleviating oxidative stress. The results showed that the levels of serum creatinine (SCr), blood urea nitrogen (BUN), and urinary protein significantly decreased in the ATL-III treatment group compared with the 5/6 nephrectomy (5/6 Nx) model group but were higher than those in the sham operation group. Skeletal muscle weight was increased, while inflammation was alleviated in the ATL-III administration group compared with the 5/6 Nx model group. ATL-III-treated rats also showed reduced dilation of the mitochondria, increased CAT, GSH-Px, and SOD activity, and decreased levels of MDA both in skeletal muscles and serum compared with 5/6 Nx model rats, suggesting that ATL-III alleviated mitochondrial damage and increased the activity of antioxidant enzymes, thus reducing the production of ROS. Furthermore, accumulated autophagosomes (APs) and autolysosomes (ALs) were reduced in the gastrocnemius (Gastroc) muscles of ATL-III-treated rats under transmission electron microscopy (TEM) together with the downregulation of LC3-II and upregulation of p62 according to Western blotting. This evidence indicated that ATL-III improved skeletal muscle atrophy and alleviated oxidative stress and autophagy in CKD rats. Furthermore, ATL-III could also increase the protein levels of p-PI3K, p-AKT, and p-mTOR in skeletal muscles in CKD rats. To further reveal the relevant mechanism, the oxidative stress-mediated PI3K/AKT/mTOR pathway was assessed, which showed that a reduced expression of p-PI3K, p-AKT, and p-mTOR in C2C12 myoblast atrophy induced by TNF-α could be upregulated by ATL-III; however, after the overexpression of Nox2 to increase ROS production, the attenuated effect was reversed. Our findings indicated that ATL-III is a potentially protective drug against muscle wasting via activation of the oxidative stress-mediated PI3K/AKT/mTOR pathway.

scholarly journals Schisandrin A protects intestinal epithelial cells from deoxynivalenol-induced cytotoxicity, oxidative damage and inflammation

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Murphy L. Y. Wan ◽  
Paul C. Turner ◽  
Vanessa A. Co ◽  
M. F. Wang ◽  
Khaled M. A. Amiri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intestinal Inflammation ◽  
Health Concern ◽  
Heme Oxygenase 1 ◽  
Antioxidant Enzyme Activities ◽  
Transferase Activity ◽  
Nuclear Factor ◽  
Ht 29

AbstractExtensive research has revealed the association of continued oxidative stress with chronic inflammation, which could subsequently affect many different chronic diseases. The mycotoxin deoxynivalenol (DON) frequently contaminates cereals crops worldwide, and are a public health concern since DON ingestion may result in persistent intestinal inflammation. There has also been considerable attention over the potential of DON to provoke oxidative stress. In this study, the cytoprotective effect of Schisandrin A (Sch A), one of the most abundant active dibenzocyclooctadiene lignans in the fruit of Schisandra chinensis (Turcz.) Baill (also known as Chinese magnolia-vine), was investigated in HT-29 cells against DON-induced cytotoxicity, oxidative stress and inflammation. Sch A appeared to protect against DON-induced cytotoxicity in HT-29 cells, and significantly lessened the DON-stimulated intracellular reactive oxygen species and nitrogen oxidative species production. Furthermore, Sch A lowered DON-induced catalase, superoxide dismutase and glutathione peroxidase antioxidant enzyme activities but maintains glutathione S transferase activity and glutathione levels. Mechanistic studies suggest that Sch A reduced DON-induced oxidative stress by down-regulating heme oxygenase-1 expression via nuclear factor (erythroid-derived 2)-like 2 signalling pathway. In addition, Sch A decreased the DON-induced cyclooxygenase-2 expression and prostaglandin E2 production and pro-inflammatory cytokine interleukin 8 expression and secretion. This may be mediated by preventing DON-induced translocation of nuclear factor-κB, as well as activation of mitogen-activated protein kinases pathways. In the light of these findings, we concluded that Sch A exerted a cytoprotective role in DON-induced toxicity in vitro, and it would be valuable to examine in vivo effects.

scholarly journals Aronia Berry Supplementation Mitigates Inflammation in T Cell Transfer-Induced Colitis by Decreasing Oxidative Stress

Nutrients ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1316 ◽  
Author(s):  
Ruisong Pei ◽  
Jiyuan Liu ◽  
Derek A. Martin ◽  
Jonathan C. Valdez ◽  
Justin Jeffety ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
T Cell ◽  
Intestinal Inflammation ◽  
H2o2 Production ◽  
Cell Transfer ◽  
Fdg Uptake ◽  
Antioxidant Function ◽  
T Cell Transfer ◽  
Gpx Activity

Oxidative stress is involved in the pathogenesis and progression of inflammatory bowel disease. Consumption of aronia berry inhibits T cell transfer colitis, but the antioxidant mechanisms pertinent to immune function are unclear. We hypothesized that aronia berry consumption could inhibit inflammation by modulating the antioxidant function of immunocytes and gastrointestinal tissues. Colitis was induced in recombinase activating gene-1 deficient (Rag1-/-) mice injected with syngeneic CD4+CD62L+ naïve T cells. Concurrent with transfer, mice consumed either 4.5% w/w aronia berry-supplemented or a control diet for five weeks. Aronia berry inhibited intestinal inflammation evidenced by lower colon weight/length ratios, 2-deoxy-2-[18F]fluoro-d-glucose (FDG) uptake, mRNA expressions of tumor necrosis factor alpha (TNF-α), and interferon gamma (IFN-γ) in the colon. Aronia berry also suppressed systemic inflammation evidenced by lower FDG uptake in the spleen, liver, and lung. Colitis induced increased colon malondialdehyde (MDA), decreased colon glutathione peroxidase (GPx) activity, reduced glutathione (rGSH) level, and suppressed expression of antioxidant enzymes in the colon and mesenteric lymph node (MLN). Aronia berry upregulated expression of antioxidant enzymes, prevented colitis-associated depletion of rGSH, and maintained GPx activity. Moreover, aronia berry modulated mitochondria-specific antioxidant activity and decreased splenic mitochondrial H2O2 production in colitic mice. Thus, aronia berry consumption inhibits oxidative stress in the colon during T cell transfer colitis because of its multifaceted antioxidant function in both the cytosol and mitochondria of immunocytes.

Intestinal Microbiota in Bone Marrow Transplantation

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. SCI-51-SCI-51
Author(s):  
Robert R. Jenq
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
Intestinal Microbiota ◽  
Marrow Transplantation ◽  
Intestinal Inflammation ◽  
Conflicts Of Interest ◽  
Allogeneic Bone Marrow Transplantation ◽  
Intestinal Flora ◽  
Intestinal Lumen ◽  
Allogeneic Bone

Abstract Abstract SCI-51 Regulators of the intestinal flora include diet, antibiotics, and importantly, intestinal inflammation. As a result, the cause-effect relationships between intestinal inflammation and changes in microbiota have been difficult to define. The success of allogeneic bone marrow transplantation (allo BMT), a standard therapy for conditions including hematopoietic malignancies and inherited hematopoietic disorders, is limited by graft-versus-host disease (GVHD) morbidity and mortality. With GVHD, vigorous activation of donor immune cells, most importantly T cells, leads to damage of the skin, liver, hematopoietic system, and gut. The major sources of immune activation are histocompatibility complex differences between donor and recipient. Combinations of chemotherapy and radiation also contribute, as damage to the intestinal epithelium results in systemic exposure to microbial products normally sequestered in the intestinal lumen. We have demonstrated in murine and human recipients of allo BMT that intestinal inflammation secondary to GVHD is associated with major shifts in the composition of the intestinal microbiota. The microbiota, in turn, can modulate the severity of intestinal inflammation. In mouse models of GVHD we observed loss of overall diversity and expansion of Lactobacillales and loss of Clostridiales. Eliminating Lactobacillales from the flora of mice prior to BMT aggravated GVHD, while reintroducing the predominant species of Lactobacillus mediated significant protection against GVHD. We then characterized the gut flora of patients during onset of intestinal inflammation due to GVHD and found patterns mirroring those in mice. We also identified increased microbial chaos soon after allo BMT as a potential risk factor for subsequent GVHD. Together, these data demonstrate regulation of flora by intestinal inflammation, and suggest that flora manipulation may reduce intestinal inflammation and improve outcomes for allo BMT recipients. Disclosures: No relevant conflicts of interest to declare.

Probiotic yeast Kluyveromyces marxianus CIDCA 8154 shows anti-inflammatory and anti-oxidative stress properties in in vivo models

2016 ◽  
Vol 7 (1) ◽  
pp. 83-93 ◽  
Author(s):  
D.E. Romanin ◽  
S. Llopis ◽  
S. Genovés ◽  
P. Martorell ◽  
V.D. Ramón ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kluyveromyces Marxianus ◽  
Intestinal Inflammation ◽  
In Vivo Models ◽  
Benzene Sulfonic Acid ◽  
Bowel Diseases ◽  
Probiotic Yeast ◽  
Anti Inflammatory

Inflammatory bowel diseases (IBDs) are complex affections with increasing incidence worldwide. Multiple factors are involved in the development and maintenance of the symptoms including enhanced oxidative stress in intestinal mucosa. The conventional therapeutic approaches for IBDs are based on the use anti-inflammatory drugs with important collateral effects and partial efficacy. In the present work we tested the anti-inflammatory capacity of Kluyveromyces marxianus CIDCA 8154 in different models. In vitro, we showed that the pretreatment of epithelial cells with the yeast reduce the levels of intracellular reactive oxygen species. Furthermore, in a murine model of trinitro benzene sulfonic acid-induced colitis, yeast-treated animals showed a reduced histopathological score (P<0.05) and lower levels of circulating interleukin 6 (P<0.05). The capacity to modulate oxidative stress in vivo was assessed using a Caenorhabditis elegans model. The yeast was able to protect the nematodes from oxidative stress by modulating the SKN-1 transcription factor trough the DAF-2 pathway. These results indicate that K. marxianus CIDCA 8154 could control the intestinal inflammation and cellular oxidative stress. Deciphering the mechanisms of action of different probiotics might be useful for the rational formulation of polymicrobial products containing microorganisms targeting different anti-inflammatory pathways.

PS2-036. How do IPEC-J2 cells function under acute oxidative stress? In vitro study on potential merit of probiotics in therapy of intestinal inflammation

Cytokine ◽  
2011 ◽  
Vol 56 (1) ◽  
pp. 73
Author(s):  
Erzsebet Pasztine Gere ◽  
Krisztina Szeker ◽  
Rita Csizinszky ◽  
Csaba Jakab ◽  
Peter Galfi
Keyword(s):  
Oxidative Stress ◽  
Intestinal Inflammation ◽  
In Vitro Study ◽  
Vitro Study

scholarly journals Serum Level of D-Lactate in Patients with Cystic Fibrosis: Preliminary Data

2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Sabina Więcek ◽  
Jerzy Chudek ◽  
Halina Woś ◽  
Maria Bożentowicz-Wikarek ◽  
Bożena Kordys-Darmolinska ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Diet Composition ◽  
Intestinal Inflammation ◽  
Clinical Symptoms ◽  
Pancreatic Insufficiency ◽  
Lactate Concentration ◽  
Intestinal Flora ◽  
International Normalized Ratio ◽  
Exocrine Pancreatic Insufficiency ◽  
Faecal Calprotectin

D-Lactate is produced by the intestinal biota and later absorbed into circulation. Some patients with cystic fibrosis (CF) develop exocrine pancreatic insufficiency that may disturb the gut microbiome and enhance the production of D-lactate. However, this concept has not been studied yet. The aim of the study was to assess D-lactate concentration in relation to the occurrence of clinical features, activity of CF, and diet composition in paediatric patients. Patients and Method. Serum concentrations of D-lactate were measured in 38 CF patients (19 girls and 19 boys) from 6 months to 18 years of age. The analysis included age, sex, clinical symptoms, diet (the variety and calorie needs), the laboratory tests for pancreatic efficiency (serum levels of albumin and glucose, faecal elastase activity, and faecal fat index) and faecal calprotectin (the marker of intestinal inflammation), and parameters of liver damage and of cholestasis (the activity of aminotransferases, γ-glutamyltransferase, level of bilirubin, and international normalized ratio). Results. The median level of D-lactate was 0.86 μg/ml (1Q–3Q: 0.48–2.03) and correlated with the CF severity in the Schwachman-Kulczycki score, parameters of pancreatic insufficiency, and the presence of intestinal inflammation. An increased level of D-lactate was observed in the subgroup with pancreas insufficiency (1.05 versus 0.73; p<0.05), parallel with an elevated level of calprotectin (0.948 versus 0.755; p=0.08). There was no relationship between energy consumption and diet composition and serum D-lactates. Conclusion. Serum D-lactate concentration in CF patients is a promising new marker of exocrine pancreatic insufficiency probably related to intestinal flora dysbiosis/overgrowth.

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