scholarly journals Anti-Inflammatory Activity of Isomaltodextrin in a C57BL/6NCrl Mouse Model with Lipopolysaccharide-Induced Low-Grade Chronic Inflammation

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2791 ◽  
Author(s):  
Hann ◽  
Zeng ◽  
Zong ◽  
Sakurai ◽  
Taniguchi ◽  
...  
Keyword(s):  
Mouse Model ◽  
Protein Expression ◽  
Tight Junction ◽  
Chronic Inflammation ◽  
Inflammatory Mediators ◽  
Macrophage Infiltration ◽  
Inflammatory Activity ◽  
Low Grade ◽  
Junction Protein ◽  
Anti Inflammatory

：The purpose of this study was to identify the anti-inflammatory activity and mechanism of isomaltodextrin (IMD) in a C57BL/6NCrl mouse model with lipopolysaccharide (LPS)-induced systemic low-grade chronic inflammation and the effect on inflammation-induced potential risk of metabolic disorders. Pre-treatment of IMD decreased the production of pro-inflammatory mediators, TNF-α and MCP-1, and stimulated the production of the anti-inflammatory mediator, adiponectin by increasing the protein expression of peroxisome proliferator-activated receptor gamma (PPAR-γ) in the white adipose tissues. IMD administration reduced plasma concentrations of endotoxin, decreased macrophage infiltration into adipocytes, and increased expression of mucin 2, mucin 4, and the tight junction protein claudin 4. These results suggest that IMD administration exerted an anti-inflammatory effect on mice with LPS-induced inflammation, potentially by decreasing circulating endotoxin, suppressing pro-inflammatory mediators and macrophage infiltration, or by improving mucus or tight junction integrity. IMD exerted protein expression of insulin receptor subset-1 (IRS-1). IMD alleviated the disturbance of gut microflora in LPS-treated mice, as the number of B. bifidum, L. casei, and B. fragilis increased, and E. coli and C. difficile decreased, when compared to LPS-treated mice. The analysis of short chain fatty acids (SCFAs) further supported that the concentrations of acetic and butyric acids were positively correlated with IMD, as well as the number of beneficial bacteria. This study provides evidence that IMD possesses anti-inflammatory properties and exerts beneficial functions to prevent systemic low-grade chronic inflammation and reduces the risk of developing insulin resistance and associated metabolic diseases.

Antioxidant and anti-inflammatory activity of a flavonoid-rich concentrate recovered from Opuntia ficus-indica juice

2014 ◽  
Vol 5 (12) ◽  
pp. 3269-3280 ◽  
Author(s):  
A. Matias ◽  
S. L. Nunes ◽  
J. Poejo ◽  
E. Mecha ◽  
A. T. Serra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Inflammation ◽  
Inflammatory Mediators ◽  
Inflammatory Activity ◽  
Oxidative Stress Biomarkers ◽  
Cactus Pear ◽  
Opuntia Ficus Indica ◽  
Stress Biomarkers ◽  
Pear Juice ◽  
Anti Inflammatory

A flavonoid-rich concentrate (FRC) recovered from cactus pear juice is able to modulate intestinal oxidative stress biomarkers and inflammatory mediators suggesting that it could be an interesting natural ingredient to attenuate and prevent intestinal chronic inflammation.

scholarly journals Beneficiary Effects of Colchicine on Inflammation and Fibrosis in A Mouse Model of Chronic Kidney Disease

2021 ◽  
Author(s):  
Daniel Landau ◽  
Nehoray Shukri ◽  
Eden Arazi ◽  
Ana Tobar ◽  
Yael Segev
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mouse Model ◽  
Macrophage Infiltration ◽  
Low Grade ◽  
Tubulin Polymerization ◽  
Mrna Levels ◽  
Caspase 1 ◽  
Inflammatory Conditions ◽  
Anti Inflammatory

Abstract Introduction: Low grade inflammation is seen in many chronic illnesses, including chronic kidney disease (CKD). We have recently reported on beneficiary effects of anti-inflammatory treatment in the interleukin (IL-)1 pathway on anemia as well as CKD extent in a mouse model. Colchicine has been shown to have beneficiary effects in several inflammatory conditions through various mechanisms, including inhibition of tubulin polymerization as well as caspase 1 mediated IL1 activation.Methods: CKD was induced by administering an adenine diet to 8-week-old C57BL/6J mice. Mice were treated with colchicine (Col) (30µg/kg) or saline injections for 3 weeks, generating 4 groups: C, C-Col, CKD and CKD-Col.Results: Uremic animals had an increase in inflammation indices in blood (neutrophils), liver and kidneys (p-STAT3, IL-6, SOCS-3). Increased kidney tubulin polymerization and caspase 1 in CKD, as well as kidney Mid88 and IRAK4 (downstream of IL1) were inhibited in CKD-Col. Kidney macrophage infiltration (F4/80 and MAC-2), the percentage of fibrotic area and TGFb mRNA levels were lower in CKD-Col Vs CKD.Conclusions: colchicine improves kidney macrophage infiltration and fibrosis in CKD through inhibition of tubulin polymerization and Caspase 1 activation. Given its reported safety profile for long term anti-inflammatory therapy without increasing infection tendency, it may serve as novel therapeutic approach in CKD.

Changes in tight junction protein expression in intrinsic aging and photoaging in human skin in vivo

2016 ◽  
Vol 84 (1) ◽  
pp. 99-101 ◽  
Author(s):  
Seon-Pil Jin ◽  
Sang Bum Han ◽  
Yeon Kyung Kim ◽  
Elizabeth Eunkyung Park ◽  
Eun Jin Doh ◽  
...  
Keyword(s):  
Protein Expression ◽  
Tight Junction ◽  
Human Skin ◽  
Tight Junction Protein ◽  
Tight Junction Protein Expression ◽  
Junction Protein

Abstract TP256: Mouse Model of Uremic Cerebral Microbleeds

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Wei Ling Lau ◽  
Mary Tarbiat-Boldaji ◽  
Hayley Smalls ◽  
Ane Nunes ◽  
Javad Savoj ◽  
...  
Keyword(s):  
Mouse Model ◽  
Tight Junction ◽  
Blood Brain Barrier ◽  
Cerebral Microbleeds ◽  
Brain Barrier ◽  
Barrier Integrity ◽  
Blood Brain ◽  
Increased Risk ◽  
Junction Protein ◽  
Blood Brain Barrier Integrity

Introduction: Cerebral microbleeds are more common in chronic kidney disease (CKD) and dialysis patients compared to the general population. Diminished kidney function alone appears to be a risk factor for microbleeds, independent of age and hypertension. Microbleed burden in CKD patients is associated with increased risk of future hemorrhagic stroke and with cognitive dysfunction. The mechanisms that drive uremic microbleed formation are unclear. Hypothesis: We hypothesized that CKD mice are predisposed to develop cerebral microhemorrhages (the pathologic substrate of microbleeds), and that a standardized inflammatory stimulus (lipopolysaccharide, LPS) will amplify microhemorrhage burden in CKD mice compared to non-CKD controls (CTL). We also hypothesized that uremia induces depletion of tight junction proteins, altering blood-brain barrier integrity and representing a potential mechanism of microbleed formation. Methods: Animal groups included CTL (n=3), CKD (n=3), CTL+LPS (n=5) and CKD+LPS (n=5). CKD induction in male C57BL/6 mice was achieved via nephrotoxic adenine diet x18 days. Two weeks following CKD induction, CKD and control mice were treated with LPS 1 mg/kg i.p. dosed at 0, 6 and 24 hours. Brains were harvested one week after LPS injections and 40-micron sections were stained using Prussian blue to identify microhemorrhages. Immunohistochemistry was performed for the blood-brain barrier tight junction protein claudin-5. Results: CKD mice had significantly elevated blood urea nitrogen, and tubulointerstitial fibrosis was present on kidney histology. Total number of microhemorrhages per brain was 2.3±1.5 (mean ± standard error of the mean) for CTL mice, 8.3±1.5 for CKD mice, 23.2±4.2 for CTL+LPS mice, and 27.6±6.2 for CKD+LPS mice (p<0.05 for CKD+LPS vs. CTL). Immunostaining showed decreased claudin-5 expression in CKD mice compared to CTL. Conclusions: We have generated a mouse model that will facilitate future mechanistic studies in the field of uremic microbleeds. Our initial findings suggest that CKD alters blood-brain barrier integrity and that inflammation amplifies development of microbleeds in CKD.

scholarly journals Dichloromethane Extracts of Geranium Koreanum Kom. Alleviates Esophagus Damage in Acute Reflux Esophagitis-Induced Rats by Anti-Inflammatory Activities

2018 ◽  
Vol 19 (11) ◽  
pp. 3622 ◽  
Author(s):  
Hyeon Nam ◽  
Li Nan ◽  
Byung Choo
Keyword(s):  
Tight Junction ◽  
Reflux Esophagitis ◽  
Mucosal Damage ◽  
Enzyme Linked Immunosorbent Assay ◽  
No Production ◽  
Esophageal Mucosa ◽  
Protective Effects ◽  
Junction Protein ◽  
Inflammatory Proteins ◽  
Anti Inflammatory

Reflux esophagitis (RE) is a gastrointestinal disease caused by the reflux of gastric acid and stomach contents, and it leads to esophageal damage. Therefore, it is necessary to study the improvement of esophageal damage on a RE-induced model. The present study was accomplished to demonstrate the protective effects of a dichloromethane fraction of Geranium koreanum (DGK) plant on esophageal damage in an acute RE rat model. First, we examined the potential of anti-inflammatory effects of various fractions measured by cell cytotoxicity, morphological changes and nitric oxide (NO) production on lipopolysaccharide (LPS)-induced Raw 264.7 macrophage cells. Then, to evaluate the protective effects on RE, rats were partitioned into the following groups: normal control, RE-induced control and RE rats pre-treated with DGK 100 and 200 mg/kg body weight. The esophageal mucosal ulcer ratio was measured by the Image J program and histological changes were examined using a hematoxylin and eosin staining of the esophageal mucosa. The expression of pro-inflammatory proteins, cytokines and tight junction proteins involved in the esophageal mucosal damage were investigated using Western blotting and an enzyme-linked immunosorbent assay (ELISA) kit with esophagus tissue. DGK chemical profile and phenolic contents were analyzed by liquid chromatography-mass spectrometry (LC-MS/MS). The results showed that DGK exhibited anti-inflammatory effects against LPS-stimulated cells by significantly inhibiting NO production. Additionally, the results in vivo showed that improvement effects of DGK on esophageal mucosal damage. The expression of inflammatory proteins involved in nuclear factor κB (NF-κB) signaling pathways and tight junction protein (claudin-4 and -5) were significantly decreased in esophageal mucosa. We found the potential of DGK as source of replacement therapy products for inflammatory and RE disease.

scholarly journals Platelet-Rich Fibrin Decreases the Inflammatory Response of Mesenchymal Cells

2021 ◽  
Vol 22 (21) ◽  
pp. 11333
Author(s):  
Zahra Kargarpour ◽  
Jila Nasirzade ◽  
Layla Panahipour ◽  
Richard J. Miron ◽  
Reinhard Gruber
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Mediators ◽  
Nuclear Translocation ◽  
Mesenchymal Cells ◽  
Pathological Process ◽  
Buffy Coat ◽  
Inflammatory Activity ◽  
Platelet Rich Fibrin ◽  
Enhanced Expression ◽  
Anti Inflammatory

Chronic inflammation is a pathological process where cells of the mesenchymal lineage become a major source of inflammatory mediators. Platelet-rich fibrin (PRF) has been shown to possess potent anti-inflammatory activity in macrophages, but its impact on mesenchymal cells has not been investigated. The aim of this study was, therefore, to expose mesenchymal cells to inflammatory cytokines together with lysates generated from liquid platelet-poor plasma (PPP), the cell-rich buffy coat layer (BC; concentrated-PRF or C-PRF), and the remaining red clot layer (RC), following centrifugation of blood. Heating PPP generates an albumin gel (Alb-gel) that when mixed back with C-PRF produces Alb-PRF. Membranes prepared from solid PRF were also subjected to lysis. We report here that lysates of PPP, BC, and PRF decreased the cytokine-induced expression of interleukin 6 (IL6) and nitric oxide synthase (iNOS) in the bone marrow-derived ST2 cells. Consistently, PPP, BC, and PRF greatly decreased the phosphorylation and nuclear translocation of p65 in ST2 cells. The inflammatory response caused by Pam3CSK4 was reduced accordingly. Moreover, PPP, BC, and PRF reduced the enhanced expression of inflammatory mediators IL6 and iNOS in 3T3-L1 pre-adipocyte mesenchymal cells, and iNOS and CCL5 in murine calvarial cells. Surprisingly, PRF lysates were not effective in reducing the inflammatory response of human gingival fibroblasts and HSC2 epithelial cells. The data from the present study suggest that both liquid PRF and solid PRF exert potent anti-inflammatory activity in murine mesenchymal cells.

Granny Smith apple procyanidin extract upregulates tight junction protein expression and modulates oxidative stress and inflammation in lipopolysaccharide-induced Caco-2 cells

2018 ◽  
Vol 9 (6) ◽  
pp. 3321-3329 ◽  
Author(s):  
H. Wu ◽  
T. Luo ◽  
Y. M. Li ◽  
Z. P. Gao ◽  
K. Q. Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Tight Junction ◽  
Tight Junction Protein ◽  
Tight Junction Protein Expression ◽  
Junction Protein

Granny Smith apple procyanidin extracts upregulate tight junction protein expression, probably acting via the modulation of oxidative stress and inflammation in lipopolysaccharide-induced Caco-2 cells.

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