scholarly journals Lung and Intestine: A Specific Link in an Ulcerative Colitis Rat Model

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Yuan Liu ◽  
Xin-Yue Wang ◽  
Xue Yang ◽  
Shan Jing ◽  
Li Zhu ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Lung Tissue ◽  
Rat Model ◽  
Close Association ◽  
Trinitrobenzene Sulfonic Acid ◽  
Microvascular Endothelium ◽  
Functional Changes ◽  
Liver And Kidney ◽  
Embryonic Origin ◽  
Endothelial Growth Factor

Background. To investigate the link and mechanisms between intestine and lung in the ulcerative colitis (UC) rat model.Materials and Methods. We used the UC rat model by immunological sensitization combined with local 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) in 50% ethanol enema, observed dynamically animal general state and body weight, examined the histological and functional changes in the colon, lung, liver, and kidney tissues, and detected microvascular endothelium response towards inflammation characterized with the expression of iNOS, TXB2, P-selectin, ICAM-1, and vascular endothelial growth factor A (VEGF-A) in the colon and lung tissue.Results. Pulmonary function results suggested ventilator disorder, and pathological findings showed interstitial pneumonia. There were no significant changes in the liver and kidney function and histopathology. The colon and lung tissue iNOS, TXB2, P-selectin, ICAM-1, and VEGF-A expression of the model rats was significantly higher than the normal rats at both time points.Conclusions. Our study is the first to demonstrate the close association between the large intestine and lung in the immune-TNBS-ethanol-induced UC rat model. Different organs and tissues with the same embryonic origin may share the same pathological specificities in a disease. The present study provided a new way of thinking for pathological changes in clinical complex diseases manifested with multiorgan damage.

scholarly journals Paradoxical regulation of ChAT and nNOS expression in animal models of Crohn's colitis and ulcerative colitis

2013 ◽  
Vol 305 (4) ◽  
pp. G295-G302 ◽  
Author(s):  
John H. Winston ◽  
Qingjie Li ◽  
Sushil K. Sarna
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Mediators ◽  
Distal Colon ◽  
Trinitrobenzene Sulfonic Acid ◽  
Mrna Levels ◽  
Functional Changes ◽  
Protein Gene Product ◽  
Dss Colitis ◽  
Nnos Expression

Morphological and functional changes in the enteric nervous system (ENS) have been reported in inflammatory bowel disease. We examined the effects of inflammation on the expression of choline acetyltransferase (ChAT) and nNOS in the muscularis externae of two models of colonic inflammation, trinitrobenzene sulfonic acid (TNBS)-induced colitis, which models Crohn's disease-like inflammation, and DSS-induced colitis, which models ulcerative Colitis-like inflammation. In TNBS colitis, we observed significant decline in ChAT, nNOS, and protein gene product (PGP) 9.5 protein and mRNA levels. In DSS colitis, ChAT and PGP9.5 were significantly upregulated while nNOS levels did not change. The nNOS dimer-to-monomer ratio decreased significantly in DSS- but not in TNBS-induced colitis. No differences were observed in the percentage of either ChAT (31 vs. 33%)- or nNOS (37 vs. 41%)-immunopositive neurons per ganglia or the mean number of neurons per ganglia (55 ± 5 vs. 59 ± 5, P > 0.05). Incubation of the distal colon muscularis externae in vitro with different types of inflammatory mediators showed that cytokines decreased ChAT and nNOS expression, whereas H2O2, a component of oxidative stress, increased their expression. NF-κB inhibitor MG-132 did not prevent the IL-1β-induced decline in either ChAT or nNOS expression. These findings showed that TNBS- and DSS-induced inflammation differentially regulates the expression of two critical proteins expressed in the colonic myenteric neurons. These differences are likely due to the exposure of the myenteric plexus neurons to different combinations of Th1-type inflammatory mediators and H2O2 in each model.

scholarly journals ShenLing BaiZhu San alleviates Ulcerative Colitis in Rats by Regulating Gut Microbiota

2020 ◽  
Author(s):  
Daxing Gu ◽  
Shanshan Zhou ◽  
Lili Yao ◽  
Ying Tan ◽  
Xingzi Chi ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Gut Microbiota ◽  
Relative Abundance ◽  
Rat Model ◽  
High Throughput Sequencing ◽  
Intestinal Barrier Function ◽  
Enzyme Linked Immunosorbent Assay ◽  
Trinitrobenzene Sulfonic Acid ◽  
Rrna Gene ◽  
Therapeutic Effects

Abstract Background: Recent studies have suggested that Shenling Baizhu San (SLBZS), an complementary and alternative medical therapy for ulcerative colitis (UC), alleviate clinic symptoms by the improvement of biochemical criteria and restoration of the intestinal barrier function. SLBZS as a famous Chinese herbal formula has been reportedly used to treat UC, of which mechanism is unknown. This study investigated the therapeutic effects of SLBZS on restoring the gut microbiota in a UC rat model. Methods: We proposed a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced UC rat model to monitor the structural modulation of the gut microbiota. The test period was 10 days (observation for two days after modeling, treatment for 8 days by SLBZS). In this study, the level of inflammatory cytokines and activity of antioxidant enzymes in serum were ascertained by enzyme-linked immunosorbent assay (ELISA) and histological changes of colon were observed. Feces were collected for high-throughput sequencing of 16S rRNA gene. Results: SLBZS partly reduced the diversity of the gut microbiota, while the abundance of that is increased. Furthermore, at the genus level, the relative abundance of short chain fatty acids (SCFA) producing bacteria including Prevotella and Oscillospira increased, while the relative abundance of harmful bacteria including Desulfovibrio, and Bilophila decreased. Additionally, SLBZS could improve the lesions of colon and significantly reduce the expression of Interleukin-6 (IL-6) and Myeloperoxidase (MPO) and increase the activities of Superoxide dismutase (SOD) and Catalase (CAT) in rats serum. Conclusions: These results demonstrate that SLBZS may treat UC effectively by inhibiting inflammation, enhancing antioxidant capacity and regulating gut microbiota.

Impaired pulmonary artery contractile responses in a rat model of microgravity: role of nitric oxide

2002 ◽  
Vol 92 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Daniel Nyhan ◽  
Soonyul Kim ◽  
Stacey Dunbar ◽  
Dechun Li ◽  
Artin Shoukas ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Pulmonary Artery ◽  
Lung Tissue ◽  
Rat Model ◽  
Orthostatic Intolerance ◽  
Volume Distribution ◽  
Contractile Responses ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Vascular contractile hyporesponsiveness is an important mechanism underlying orthostatic intolerance after microgravity. Baroreceptor reflexes can modulate both pulmonary resistance and capacitance function and thus cardiac output. We hypothesized, therefore, that pulmonary vasoreactivity is impaired in the hindlimb-unweighted (HLU) rat model of microgravity. Pulmonary artery (PA) contractile responses to phenylephrine (PE) and U-46619 (U4) were significantly decreased in the PAs from HLU vs. control (C) animals. N G-nitro-l-arginine methyl ester (10−5 M) enhanced the contractile responses in the PA rings from both C and HLU animals and completely abolished the differential responses to PE and U4 in HLU vs. C animals. Vasorelaxant responses to ACh were significantly enhanced in PA rings from HLU rats compared with C. Moreover, vasorelaxant responses to sodium nitroprusside were also significantly enhanced. Endothelial nitric oxide synthase (eNOS) and soluble guanlyl cyclase expression were significantly enhanced in PA and lung tissue from HLU rats. In marked contrast, the expression of inducible nitric oxide synthase was unchanged in lung tissue. These data support the hypothesis that vascular contractile responsiveness is attenuated in PAs from HLU rats and that this hyporesponsiveness is due at least in part to increased nitric oxide synthase activity resulting from enhanced eNOS expression. These findings may have important implications for blood volume distribution and attenuated stroke volume responses to orthostatic stress after microgravity exposure.

Hyperpolarized 129Xe Magnetic Resonance Spectroscopy in a Rat Model of Bronchopulmonary Dysplasia

2021 ◽  
Author(s):  
Jordan David Fliss ◽  
Brandon Zanette ◽  
Yonni Friedlander ◽  
Siddharth Sadanand ◽  
Andras A Lindenmaier ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Gas Exchange ◽  
Magnetic Resonance Spectroscopy ◽  
Bronchopulmonary Dysplasia ◽  
Rat Model ◽  
Resonance Spectroscopy ◽  
Gas Exchange Parameters ◽  
Functional Changes ◽  
Non Invasive

Premature infants often require mechanical ventilation and oxygen therapy which can result in bronchopulmonary dysplasia (BPD), characterized by developmental arrest and impaired lung function. Conventional clinical methods for assessing the prenatal lung are not adequate for the detection and assessment of long-term health risks in infants with BPD, highlighting the need for a non-invasive tool for the characterization of lung microstructure and function. Theoretical diffusion models, like the Model of Xenon Exchange (MOXE), interrogate alveolar gas exchange by predicting the uptake of inert Hyperpolarized (HP) 129Xe gas measured with HP 129Xe magnetic resonance spectroscopy (MRS). To investigate HP 129Xe MRS as a tool for non-invasive characterization of pulmonary microstructural and functional changes in vivo, HP 129Xe gas exchange data were acquired in an oxygen exposure rat model of BPD that recapitulates the fewer and larger distal airways and pulmonary vascular stunting characteristics of BPD. Gas exchange parameters from MOXE, including airspace mean chord length (L­m), apparent hematocrit in the pulmonary capillaries (HCT), and pulmonary capillary transit time (tx), were compared with airspace mean axis length and area density (MAL and ρ­A) and percentage area of tissue and air (PTA and PAA) from histology. L­m was significantly larger in the exposed rats (p=0.003) and correlated with MAL, ρ­A, PTA, and PAA (0.59<|ρ|<0.66 and p<0.05). Observed increase in HCT (p=0.012) and changes in tx are also discussed. These findings support the use of HP 129Xe MRS for detecting fewer, enlarged distal airways in this rat model of BPD, and potentially in humans.

scholarly journals Mouse model of ulcerative colitis using trinitrobenzene sulfonic acid

2015 ◽  
Vol 10 (4) ◽  
pp. 860
Author(s):  
Irfan Ahmad Rather ◽  
Vivek K. Bajpai ◽  
Nam Gyeong-Jun
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Mouse Model ◽  
Bowel Disease ◽  
Sulfonic Acid ◽  
Intestinal Inflammation ◽  
Cost Effective ◽  
Trinitrobenzene Sulfonic Acid ◽  
Clinical Presentations ◽  
Inflammatory Bowel

<p>Animal model of intestinal inflammation is of paramount significance that aids in discerning the pathologies underlying ulcerative colitis and Crohn’s disease, the two clinical presentations of inflammatory bowel disease. The 2,4,6-trinitrobenzene sulfonic acid (TNBS) colitis model represents one such intestinal inflammation-prototype that is generated in susceptible strains of mice through intra-rectal instillation of compound TNBS. In this paper, we demonstrate the experimental induction of TNBS-mediated colitis in a susceptible strain of ICR mice. This can be done by the following steps: a) acclimation, b) induction and c) observation. TNBS-mouse model provides the information in shortest possible time and simultaneously represents a cost effective and highly reproducible model method of studying the pathogenesis of inflammatory bowel disease.</p><p><strong>Video Clips</strong></p><p><a href="https://youtube.com/v/6MsuIGzH3uA">Acclimation and induction of TNBS</a>:          4.5 min</p><p><a href="https://youtube.com/v/ya66SNwoVag">Observation and drug administration</a>:      1.5 min</p>

scholarly journals Influence of distal ileum exclusion on hepatic and renal functions in presence of extrahepatic cholestasis

2014 ◽  
Vol 41 (2) ◽  
pp. 112-116
Author(s):  
Evandro Luis de Oliveira Costa ◽  
Andy Petroianu ◽  
Geraldo Magela de Azevedo Júnior
Keyword(s):  
Terminal Ileum ◽  
Biliary Drainage ◽  
Hepatic Duct ◽  
Control Group ◽  
Extrahepatic Cholestasis ◽  
Functional Changes ◽  
Duct Ligation ◽  
Liver And Kidney ◽  
Group 3 ◽  
Group 1

OBJECTIVE: To verify whether the ileal exclusion interferes with liver and kidney functional changes secondary to extrahepatic cholestasis.METHODS: We studied 24 rats, divided into three groups with eight individuals each: Group 1 (control), Group 2 (ligation of the hepatic duct combined with internal biliary drainage), and Group 3 (bile duct ligation combined with internal biliary drainage and exclusion of the terminal ileum). Animals in Group 1 (control) underwent sham laparotomy. The animals of groups 2 and 3 underwent ligation and section of the hepatic duct and were kept in cholestasis for four weeks. Next, they underwent an internal biliary bypass. In Group 3, besides the biliary-enteric bypass, we associated the exclusion of the last ten centimeters of the terminal ileum and carried out an ileocolic anastomosis. After four weeks of monitoring, blood was collected from all animals of the three groups for liver and kidney biochemical evaluation (albumin, ALT, AST, direct and indirect bilirubin, alkaline phosphatase, cGT, creatinine and urea).RESULTS: there were increased values of ALT, AST, direct bilirubin, cGT, creatinine and urea in rats from Group 3 (p < 0.05).CONCLUSION: ileal exclusion worsened liver and kidney functions in the murine model of extrahepatic cholestasis, being disadvantageous as therapeutic procedure for cholestatic disorders.

scholarly journals Changes in Gene Expression in Rat Tissues during Toxoplasmosis

2021 ◽  
Vol 6 (2) ◽  
pp. 236-241
Author(s):  
E. S. Pashinskaya ◽  
Keyword(s):  
Gene Expression ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Lung Tissue ◽  
Rat Tissues ◽  
Vascular Endothelial ◽  
Epidermal Growth ◽  
Endothelial Growth Factor ◽  
Brain Tissues

The purpose of the study is to study changes in gene expression in rat tissues during toxoplasmosis. Materials and methods. The experiment was conducted on 70 Wistar females weighing 170-220 grams. To achieve this goal, the expression of the proto-oncogenes survivin (BIRC5), epidermal growth factor (ErbB-2/HER2-Neu), GLI, vascular endothelial growth factor (VEGF) and anti-oncogene TP53 was determined in comparison with the reference genes β-actin (ACTB) and GAPDH by PCR analysis in the tissues of 10 healthy female rats and 60 infected with toxoplasma. RNA isolation was performed by the column method using the ReliaPrep RNA Cell Miniprep System (Promega Corporation, USA). The quality of the isolated RNA was evaluated spectrophotometrically. Reverse transcription was performed using M-MuLV RT (New England BioLabs Inc, USA). Primers specific to the genes were prepared using Primer3 and the NCBI Nucleotide database. Amplification was performed on a Real-Time PCR Detection System CFX96 thermal cycler (Bio-Rad, USA), using a qPCRmix-HS SYBR PCR mixture (Eurogen, Russia). Comparative expression of the studied genes was carried out after normalization of each of the samples to the level of the control genes GAPDH and ACTIN-β. Expression analysis was performed by qbase+ and CFX Maestro. Statistical processing of the obtained data was carried out using the program Statistica 10.0. Results and discussion. Toxoplasma increases the expression of survivin (BIRC5) in lung tissue to 0.013 relative units, in liver – to 0.038 relative units, in spleen – to 0.061 relative units, and in brain – to 0.050 relative units. VEGF expression in lungs increased to 0.034 relative units, in liver – to 0.041 relative units, in spleen – to 0.063 relative units, in brain tissues – to 0.080 relative units. There was an increase in the expression of ErbB-2/HER2-Neu in lung tissue to 0.436 relative units, in liver – to 0.259 relative units, in spleen – to 0.271 relative units, and in brain – to 0.131 relative units. GLI expression in lung tissues after toxoplasma infection increased to 0.113 relative units, in liver – to 0.188 relative units, in spleen – to 0.388 relative units, and in brain tissues – to 0.459 relative units. An increase in the expression of the anti-oncogene TP53 in the tissues of the lungs to 0.171 relative units, liver – to 0.295, spleen – to 0.408, and brain – to 0.259 relative units was revealed. Conclusion. It has been shown that toxoplasma can cause an increase in the expression of the proto-oncogenes survivin (BIRC5), epidermal growth factor (ErbB-2/HER2-Neu), GLI and vascular endothelial growth factor (VEGF) with simultaneous enhancement of the anti-oncogene TP53

scholarly journals Modulation of Oxidative and Nitrosative Stress Attenuates Microvascular Hyperpermeability in Ovine Model of Pseudomonas Aeruginosa Sepsis

2021 ◽  
Author(s):  
Satoshi Fukuda ◽  
Yosuke Niimi ◽  
Yasutaka Hirasawa ◽  
Ennert R. Manyeza ◽  
C. Edwin Garner ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Pseudomonas Aeruginosa ◽  
Growth Factor ◽  
Lung Tissue ◽  
Interleukin 6 ◽  
Nitrosative Stress ◽  
Vascular Endothelial ◽  
Ovine Model ◽  
Organ Function ◽  
Endothelial Growth Factor

Abstract Background: Sepsis is one of the most frequent causes of death in the ICU, and microvascular hyperpermeability caused by oxidative/nitrosative stress plays an important role in tissue edema leading to multi-organ dysfunctions and increased mortality. This study tested the efficacy of a novel compound R-107, a modulator of oxidative/nitrosative stress, in an ovine model of sepsis. We hypothesized that R-107 effectively ameliorates the severity of microvascular hyperpermeability and preserves multi-organ function.Methods: Sepsis was induced in twenty-two adult female Merino sheep by intravenous infusion of Pseudomonas aeruginosa (1x1010 CFUs) for 60 minutes. After injury, animals were allocated into the following groups: 1) Control: intramuscular injection (IM) of saline, n=13; and 2) Treatment: IM of 50 mg/kg R-107, n=9. The IM treatment was given after the completion of the Pseudomonas aeruginosa injection. Animals were placed on a mechanical ventilator, fluid resuscitated, and monitored for 24 hours in a conscious state. Results: R-107 treatment attenuated 24-hour mortality (11 vs. 30%). R-107 significantly reduced fluid requirement (15 – 24 hours, p<0.05), net fluid balance (9 – 24 hours, p<0.05), and water content in lung, heart, and kidney (p=0.02, 0.04, and 0.01, respectively) compared to control. R-107 treatment significantly delayed the onset of positive qSOFA (3.3 vs. 6.8 hours, p=0.04), and significantly decreased lung injury score and modified sheep SOFA score at 24 hours (p=0.01 and 0.04). The R-107 treatment group had significantly lower arterial lactate (21 – 24 hours, p<0.05), shed syndecan-1 (3 – 6 hours, p<0.05), and interleukin-6 (6 – 12 hours, p<0.05) levels in plasma, and significantly attenuated lung tissue 3-nitrotyrosine and vascular endothelial growth factor-A expression (p=0.03 and 0.002) compared to control. There was no adverse effect observed during R-107 treatment.Conclusions: Modulation of oxidative/nitrosative stress by R-107 reduced lung tissue vascular endothelial growth factor-A, plasma shed syndecan-1, and interleukin-6 and attenuated severe microvascular hyperpermeability resulting in improved multi-organ function and survival in Pseudomonas aeruginosa sepsis.

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