scholarly journals Emu Oil Reduces Small Intestinal Inflammation in the Absence of Clinical Improvement in a Rat Model of Indomethacin-Induced Enteropathy

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Suzanne M. Abimosleh ◽  
Cuong D. Tran ◽  
Gordon S. Howarth
Keyword(s):  
Intestinal Inflammation ◽  
Activity Index ◽  
Disease Activity Index ◽  
Intestinal Damage ◽  
Sprague Dawley ◽  
Emu Oil ◽  
Sprague Dawley Rats ◽  
Nsaid Enteropathy ◽  
Small Intestinal ◽  
Normal Controls

Nonsteroidal-anti-inflammatory-drug (NSAID) enteropathy is characterized by small intestinal damage and ulceration. Emu Oil (EO) has previously been reported to reduce intestinal inflammation.Aim. We investigated EO for its potential to attenuate NSAID-enteropathy in rats.Methods. Male Sprague Dawley rats (n=10/group) were gavaged with Water, Olive Oil (OO), or EO (0.5 mL; days 0–12) and with 0.5 mL Water or the NSAID, Indomethacin (8 mg/kg; days 5–12) daily. Disease activity index (DAI), 13C-sucrose breath test (SBT), organ weights, intestinal damage severity (IDS), and myeloperoxidase (MPO) activity were assessed.P<0.05was considered significant.Results. In Indomethacin-treated rats, DAI was elevated (days 10–12) and SBT values (56%) and thymus weight (55%) were decreased, relative to normal controls. Indomethacin increased duodenum (68%), colon (24%), SI (48%), caecum (48%), liver (51%) and spleen (88%) weights, IDS scores, and MPO levels (jejunum: 195%, ileum: 104%) compared to normal controls. Jejunal MPO levels were decreased (64%) by both EO and OO, although only EO decreased ileal MPO (50%), compared to Indomethacin controls.Conclusions. EO reduced acute intestinal inflammation, whereas other parameters of Indomethacin-induced intestinal injury were not affected significantly. Increased EO dose and/or frequency of administration could potentially improve clinical efficacy.

scholarly journals Glycomacropeptide Ameliorates Indomethacin-Induced Enteropathy in Rats by Modifying Intestinal Inflammation and Oxidative Stress

Molecules ◽  
2020 ◽  
Vol 25 (10) ◽  
pp. 2351 ◽  
Author(s):  
Daniel Cervantes-García ◽  
Armida I. Bahena-Delgado ◽  
Mariela Jiménez ◽  
Laura E. Córdova-Dávalos ◽  
Vanessa Ruiz-Esparza Palacios ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Intestinal Inflammation ◽  
Biological Activities ◽  
Antioxidant Properties ◽  
Lipid Hydroperoxide ◽  
Neutrophil Infiltration ◽  
Clinical Problem ◽  
Intestinal Damage ◽  
Nsaid Enteropathy ◽  
Anti Inflammatory

Nonsteroidal anti-inflammatory drug (NSAID)-induced enteropathy is considered a serious and increasing clinical problem without available treatment. Glycomacropeptide (GMP) is a 64-amino acid peptide derived from milk κ-casein with numerous biological activities. The aim of this study was to investigate the protective effect of GMP on NSAID enteropathy in rats. Enteropathy was induced by seven days oral indomethacin administration. Rats were orally GMP treated from seven days previous and during the establishment of the enteropathy model. Changes in metabolism, hematological and biochemical blood alterations, intestinal inflammation and oxidative damage were analyzed. Integrity barrier markers, macroscopic intestinal damage and survival rate were also evaluated. GMP treatment prevented anorexia and weight loss in animals. Furthermore, prophylaxis with GMP ameliorated the decline in hemoglobin, hematocrit, albumin and total protein levels. The treatment had no therapeutic efficacy on the decrease of occludin and mucin (MUC)-2 expression in intestinal tissue. However, GMP markedly decreased neutrophil infiltration, and CXCL1, interleukin-1β and inducible nitric oxide synthase expression. Nitric oxide production and lipid hydroperoxide level in the small intestine were also diminished. These beneficial effects were mirrored by preventing ulcer development and increasing animal survival. These results suggest that GMP may protect against NSAID enteropathy through anti-inflammatory and antioxidant properties.

scholarly journals Isolation and Characterization of Potentially Probiotic Bacterial Strains from Mice: Proof of Concept for Personalized Probiotics

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1684 ◽  
Author(s):  
Larissa Celiberto ◽  
Roseli Pinto ◽  
Elizeu Rossi ◽  
Bruce Vallance ◽  
Daniela Cavallini
Keyword(s):  
Intestinal Inflammation ◽  
Activity Index ◽  
Disease Activity Index ◽  
Bacterial Strains ◽  
Dss Colitis ◽  
Isolation And Characterization ◽  
Inflammatory Bowel ◽  
Commercial Probiotics ◽  
Lower Disease Activity

Modulation of the gut microbiota through the use of probiotics has been widely used to treat or prevent several intestinal diseases. However, inconsistent results have compromised the efficacy of this approach, especially in severe conditions such as inflammatory bowel disease (IBD). The purpose of our study was to develop a personalized probiotic strategy and assess its efficacy in a murine model of intestinal inflammation. Commensal bacterial strains were isolated from the feces of healthy mice and then administered back to the host as a personalized treatment in dextran sodium sulfate (DSS)-induced colitis. Colonic tissues were collected for histological analysis and to investigate inflammatory markers such as Il-1β, Il-6, TGF-β, and Il-10, and the enzyme myeloperoxidase as a neutrophil marker. The group that received the personalized probiotic showed reduced susceptibility to DSS-colitis as compared to a commercial probiotic. This protection was characterized by a lower disease activity index and reduced histopathological damage in the colon. Moreover, the personalized probiotic was more effective in modulating the host immune response, leading to decreased Il-1β and Il-6 and increased TGF-β and Il-10 expression. In conclusion, our study suggests that personalized probiotics may possess an advantage over commercial probiotics in treating dysbiotic-related conditions, possibly because they are derived directly from the host’s own microbiota.

scholarly journals Huangkui Lianchang Decoction Ameliorates DSS-Induced Ulcerative Colitis in Mice by Inhibiting the NF-kappaB Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Zongqi He ◽  
Qing Zhou ◽  
Ke Wen ◽  
Bensheng Wu ◽  
Xueliang Sun ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Western Blot ◽  
Signaling Pathway ◽  
Intestinal Inflammation ◽  
Activity Index ◽  
Quantitative Polymerase Chain Reaction ◽  
Comparable Efficacy ◽  
Intestinal Damage ◽  
Macroscopic Lesion ◽  
Cox 2

Background. The nuclear factor kappa beta (NF-κB) signaling pathway plays an important role in ulcerative colitis (UC). Huangkui Lianchang decoction (HLD) is an effective traditional Chinese medicinal compound used in the treatment of UC. HLD has good effects in the clinic, but the mechanism by which HLD acts is unclear. This study aims to reveal the exact molecular mechanism of HLD in the treatment of UC. Methods. Mouse ulcerative colitis was induced by dextran sulfate sodium (DSS) and treated with HLD. Intestinal damage was assessed by disease activity index (DAI), colon macroscopic lesion scores, and histological scores. Interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-1β were detected in colon tissue using ELISA. Myeloperoxidase (MPO) and superoxide dismutase (SOD) activities in the colonic mucosa were measured. The levels of IL-6, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) in the colon were determined by real-time quantitative polymerase chain reaction (qPCR). The expression of NF-κB, IκBα, and p-IκBα in the colon was measured by Western blot. Results. After treatment with HLD, the DAI scores, macroscopic lesion scores, and histological scores decreased, and the levels of inflammatory cytokines related to the NF-κB signaling pathway, such as IL-6, TNF-α, and IL-1β, as well as those of iNOS and COX-2, were reduced; at the same time, colonic pathological damage was alleviated, and the MPO and SOD activities decreased. Western blot confirmed that HLD can inhibit the NF-κB signaling pathway in DSS-induced ulcerative colitis. Conclusion. HLD can alleviate the inflammation caused by ulcerative colitis. In particular, high doses of HLD can significantly alleviate intestinal inflammation and have comparable efficacy to Mesalazine. We propose that the anti-inflammatory activity of HLD on DSS-induced colitis in mice may involve the inhibition of the NF-κB pathway.

Effects of antecedent hypoglycemia, hyperinsulinemia, and excess corticosterone on hypoglycemic counterregulation

2001 ◽  
Vol 281 (3) ◽  
pp. E455-E465 ◽  
Author(s):  
Kathy Shum ◽  
Karen Inouye ◽  
Owen Chan ◽  
Julian Mathoo ◽  
Debra Bilinski ◽  
...  
Keyword(s):  
Autonomic Failure ◽  
Glucose Production ◽  
Hyperinsulinemic Hypoglycemia ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Per Se ◽  
Normal Controls

This study aimed to differentiate the effects of repeated antecedent hypoglycemia, antecedent marked hyperinsulinemia, and antecedent increases in corticosterone on counterregulation to subsequent hypoglycemia in normal rats. Specifically, we examined whether exposure to hyperinsulinemia or elevated corticosterone per se could impair subsequent counterregulation. Four groups of male Sprague-Dawley rats were used: 1) normal controls (N) had 4 days of sham antecedent treatment; 2) an antecedent hypoglycemia group (AH) had 7 episodes of hyperinsulinemic hypoglycemia over 4 days; 3) an antecedent hyperinsulinemia group (AE) had 7 episodes of hyperinsulinemic euglycemia; and 4) an antecedent corticosterone group (AC) had 7 episodes of intravenous corticosterone to simulate the hypoglycemic corticosterone levels in AH rats. On day 5, hyperinsulinemic euglycemic-hypoglycemic clamps were performed. Epinephrine responses to hypoglycemia were impaired ( P< 0.05 vs. N) after antecedent hypoglycemia and hyperinsulinemia. This correlated with diminished ( P < 0.05 vs. N) absolute glucose production responses in AH rats and diminished incremental glucose production responses in AE rats. Paradoxically, norepinephrine responses were increased ( P < 0.05 vs. N) after antecedent hypoglycemia. Glucagon and corticosterone responses were unaffected by antecedent hypoglycemia and hyperinsulinemia. In AC rats, incremental but not absolute glucose production responses were decreased ( P < 0.05 vs. N). However, neuroendocrine counterregulation was unaltered. We conclude that both antecedent hypoglycemia and hyperinsulinemia impair epinephrine and glucose production responses to subsequent hypoglycemia, suggesting that severe recurrent hyperinsulinemia may contribute to the development of hypoglycemia-associated autonomic failure.

scholarly journals Effects of realimentation on small intestinal morphology and disaccharidase activity in malnutrition Sprague-Dawley rats

2006 ◽  
pp. 208
Author(s):  
Rustadi Sosrosumihardjo ◽  
Agus Firmansyah ◽  
Asri Rasad ◽  
Daldiyono Harjodisastro ◽  
Endi Ridwan ◽  
...  
Keyword(s):  
Intestinal Morphology ◽  
Sprague Dawley ◽  
Disaccharidase Activity ◽  
Sprague Dawley Rats ◽  
Small Intestinal

scholarly journals Use Of The Prebiotic Inulin In The Prevention Of Adverse Signs Of Acute Colitis

2015 ◽  
Vol 65 (3) ◽  
pp. 339-347
Author(s):  
Hijová Emília ◽  
Śoltésová Alena ◽  
Salaj Rastislav ◽  
Kuzma Jozef ◽  
Strojný Ladislav ◽  
...  
Keyword(s):  
Activity Index ◽  
Disease Activity Index ◽  
Coliform Bacteria ◽  
Control Group ◽  
Sprague Dawley ◽  
Acute Colitis ◽  
Colon Tissue ◽  
Diet Intervention ◽  
Average Value ◽  
Glucuronidase Activity

Abstract The aim of this study was to investigate the influence of prebiotic inulin diet intervention on the activity of β-glucuronidase and counts of coliforms and lactobacilli in fresh caecal digesta, cytokine levels (IL-6, IL-8) and transcription nuclear factor kappa beta (NFkB) activities in the colon tissue and blood samples of rats with dextran sulphate sodium (DSS) induced acute colitis. Male Sprague-Dawley rats (8 per group) were randomly divided into three groups: Control, Acute colitis and Prebiotic. Colitis was induced using 5% DSS in drinking water for 7d. DSS application significantly increased the activity of β-glucuronidase (p<0.001), increased counts of coliform bacteria and decreased lactobacilli count (p<0.05) in comparison to the control group. Serum and tissue levels of IL-6 and IL-8 as well as tissue NFkB activities showed an increased expression in the acute colitis group. These results correspond to the average value of the disease activity index score (DAI) and revealed the maximum DAI score (6.5) in the acute colitis group. A decrease in the DAI score (4.13) was observed after application of the prebiotic inulin. Inulin diet intervention positively modified the number of microorganims and decreased β-glucuronidase activity. Colon tissue activities of NFkB were significantly suppressed (p<0.001). The synthesis of proinflammatory cytokines IL-6 (p<0.01) in the serum and in the colon tissue, as well as tissue IL-8 (p<0.05) in the prebiotic group were downregulated. These findings indicate that the dietary intake of inulin suppressed the expression of the observed markers, which play an important role in the inflammatory process, which predisposes to the use of inulin in the prevention or treatment of acute colitis in human and veterinary medicine.

scholarly journals Hyperosmolarity in the small intestine contributes to postprandial ghrelin suppression

2014 ◽  
Vol 306 (12) ◽  
pp. G1108-G1116 ◽  
Author(s):  
Joost Overduin ◽  
Tracy S. Tylee ◽  
R. Scott Frayo ◽  
David E. Cummings
Keyword(s):  
Small Intestine ◽  
Glucose Solution ◽  
Jugular Vein ◽  
Gastric Bypass Surgery ◽  
Sprague Dawley ◽  
Macronutrient Composition ◽  
Sprague Dawley Rats ◽  
Small Intestinal ◽  
The Impact ◽  
Dietary Modifications

Plasma levels of the orexigenic hormone ghrelin are suppressed by meals with an efficacy dependent on their macronutrient composition. We hypothesized that heterogeneity in osmolarity among macronutrient classes contributes to these differences. In three studies, the impact of small intestinal hyperosmolarity was examined in Sprague-Dawley rats. In study 1, isotonic, 2.5×, and 5× hypertonic solutions of several agents with diverse absorption and metabolism properties were infused duodenally at a physiological rate (3 ml/10 min). Jugular vein blood was sampled before and at 30, 60, 90, 120, 180, 240, and 300 min after infusion. Plasma ghrelin was suppressed dose dependently and most strongly by glucose. Hyperosmolar infusions of lactulose, which transits the small intestine unabsorbed, and 3- O-methylglucose (3- O-MG), which is absorbed like glucose but remains unmetabolized, also suppressed ghrelin. Glucose, but not lactulose or 3- O-MG, infusions increased plasma insulin. In study 2, intestinal infusions of hyperosmolar NaCl suppressed ghrelin, a response that was not attenuated by coinfusion with the neural blocker lidocaine. In study 3, we reconfirmed that the low-osmolar lipid emulsion Intralipid suppresses ghrelin more weakly than isocaloric (but hypertonic) glucose. Importantly, raising Intralipid's osmolarity to that of the glucose solution by nonabsorbable lactulose supplementation enhanced ghrelin suppression to that seen after glucose. Hyperosmolar ghrelin occurred particularly during the initial 3 postinfusion hours. We conclude that small intestinal hyperosmolarity 1) is sufficient to suppress ghrelin, 2) may combine with other postprandial mechanisms to suppress ghrelin, 3) might contribute to altered ghrelin regulation after gastric bypass surgery, and 4) may inform dietary modifications for metabolic health.

scholarly journals Identification of transient glycosylation alterations of sialylated mucin oligosaccharides during infection by the rat intestinal parasite Nippostrongylus brasiliensis

2000 ◽  
Vol 350 (3) ◽  
pp. 805-814 ◽  
Author(s):  
Niclas G. KARLSSON ◽  
Fredrik J. OLSON ◽  
Per-Åke JOVALL ◽  
Ylva ANDERSCH ◽  
Lennart ENERBÄCK ◽  
...  
Keyword(s):  
Infection Process ◽  
Nippostrongylus Brasiliensis ◽  
Blood Group Antigens ◽  
Intestinal Infection ◽  
Sprague Dawley ◽  
Acetylneuraminic Acid ◽  
Sprague Dawley Rats ◽  
Small Intestinal ◽  
Infectious Cycle ◽  
Intestinal Mucins

The sialylation of the oligosaccharides from small-intestinal mucins during a 13-day infectious cycle was studied in Sprague–Dawley rats with the parasite Nippostrongylus brasiliensis. Sialic acid analysis and release, permethylation and analysis by GC-MS of the sialylated oligosaccharides isolated from the ‘insoluble’ mucin complex revealed a relative decrease (4–7-fold) of N-glycolylneuraminic acid compared with N-acetylneuraminic acid just before parasite expulsion. Northern blots showed that this effect was due to the decreased expression of a hydroxylase converting CMP-N-acetylneuraminic acid into CMP-N-glycolylneuraminic acid. Analysis of other rat strains showed that this parasite infection also caused the same effect in these animals. Detailed analysis of infected Sprague–Dawley rats revealed four sialylated oligosaccharides not found in the uninfected animals. These new oligosaccharides were characterized in detail and all shown to contain the trisaccharide epitope NeuAc/NeuGcα2-3(GalNAcβ1-4)Galβ1 (where NeuGc is N-glycolyl neuraminic acid). This epitope is similar to the Sda- and Cad-type blood-group antigens and suggests that the infection causes the induction of a GalNAcβ1-4 glycosyltransferase. This model for an intestinal infection suggests that the glycosylation of intestinal mucins is a dynamic process being modulated by the expression of specific enzymes during an infection process.

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