scholarly journals Inflammatory bowel and oxidative stress changes in an experimental model of portal hypertension: action of N-acetylcysteine

2016 ◽  
Vol 36 (4) ◽  
pp. 231-239 ◽  
Author(s):  
Francielli Licks ◽  
Renata Minuzzo Hartmann ◽  
Elizângela Schemitt ◽  
Josieli Raskopf Colares ◽  
Lúcio Sarubbi Fillmann ◽  
...  
Life Sciences ◽  
2021 ◽  
Vol 272 ◽  
pp. 119194
Author(s):  
Diva de Aguiar Magalhães ◽  
Jalles Arruda Batista ◽  
Stefany Guimarães Sousa ◽  
Jayro dos Santos Ferreira ◽  
Lauanda da Rocha Rodrigues ◽  
...  

Inflammation ◽  
2020 ◽  
Vol 43 (4) ◽  
pp. 1411-1422
Author(s):  
S. Sheethal ◽  
M. Ratheesh ◽  
Svenia P. Jose ◽  
S. Asha ◽  
I. M. Krishnakumar ◽  
...  

2018 ◽  
Vol 8 ◽  
Author(s):  
Leandro do Nascimento Camargo ◽  
Renato Fraga Righetti ◽  
Luciana Ritha de Cássia Rolim Barbosa Aristóteles ◽  
Tabata Maruyama dos Santos ◽  
Flávia Castro Ribas de Souza ◽  
...  

2009 ◽  
Vol 44 (1) ◽  
pp. 74-89 ◽  
Author(s):  
Rosanna di Paola ◽  
Emanuela Esposito ◽  
Emanuela Mazzon ◽  
Rocco Caminiti ◽  
Roberto Dal Toso ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
N. F. Renna ◽  
C. Lembo ◽  
E. Diez ◽  
R. M. Miatello

(1) This study aims to demonstrate the causal involvement of renin angiotensin system (RAS) and oxidative stress (OS) on vascular inflammation in an experimental model of metabolic syndrome (MS) achieved by fructose administration to spontaneously hypertensive rats (FFHR) during 12 weeks. (2) Chronic treatment with candesartan (C) (10 mg/kg per day for the last 6 weeks) or 4OH-Tempol (T) (10−3 mmol/L in drinking water for the last 6 weeks) reversed the increment in metabolic variables and systolic blood pressure. In addition, chronic C treatment reverted cardiovascular remodeling but not T. (3) Furthermore, chronic treatment with C was able to completely reverse the expression of NF-κB and VCAM-1, but T only reduced the expression. C reduced the expression of proatherogenic cytokines as CINC2, CINC3, VEGF, Leptin, TNF-alpha, and MCP-1 and also significantly reduced MIP-3, beta-NGF, and INF-gamma in vascular tissue in this experimental model. T was not able to substantially modify the expression of these cytokines. (4) The data suggest the involvement of RAS in the expression of inflammatory proteins at different vascular levels, allowing the creation of a microenvironment suitable for the creation, perpetuation, growth, and destabilization of vascular injury.


2004 ◽  
Vol 260 (1) ◽  
pp. 21-29 ◽  
Author(s):  
Pawan K. Singal ◽  
Firoozeh Farahmand ◽  
Michael F. Hill

2016 ◽  
Vol 157 (45) ◽  
pp. 1781-1785 ◽  
Author(s):  
Iván Péter ◽  
Anna Jagicza ◽  
Zénó Ajtay ◽  
István Kiss ◽  
Balázs Németh

Psoriasis is among the most common dermatological diseases worldwide. Its significance is emphasized by adverse effects on quality of life, caused by chronic pain, physical and psychical disability due to psoriatic plaques. Besides the development of psoriatic arthritis, which often causes permanent joint damage, former studies revealed an increased risk of inflammatory bowel disease, cardiovascular disease and certain types of cancer. Genetic predisposition and oxidative stress caused by exogenous and endogenous factors can contribute to abnormal differentiation and hyperproliferation of keratinocytes, accordingly the development and maintenance of psoriasis. Moreover, excessive oxidative stress can be responsible for the onset of psoriasis complications. After a brief pathophysiological summary the authors discuss the role of oxidative stress in the development of psoriasis and its complications through several well studied biomarkers (asymmetric dimethylarginine, malondialdehyde, superoxide dismutase, catalase). Orv. Hetil., 2016, 157(45), 1781–1785.


2016 ◽  
Vol 10 (10) ◽  
pp. 2389-2404 ◽  
Author(s):  
Nicholas Edward Ilott ◽  
Julia Bollrath ◽  
Camille Danne ◽  
Chris Schiering ◽  
Matthew Shale ◽  
...  

Abstract The gut microbiome is significantly altered in inflammatory bowel diseases, but the basis of these changes is not well understood. We have combined metagenomic and metatranscriptomic profiling of the gut microbiome to assess modifications to both bacterial community structure and transcriptional activity in a mouse model of colitis. By using transcriptomic analysis of colonic tissue and luminal RNA derived from the host, we have also characterised how host transcription relates to the microbial transcriptional response in inflammation. In colitis, increased abundance and transcription of diverse microbial gene families involved in responses to nutrient deprivation, antimicrobial peptide production and oxidative stress support an adaptation of multiple commensal genera to withstand a diverse set of environmental stressors in the inflammatory environment. These data are supported by a transcriptional signature of activated macrophages and granulocytes in the gut lumen during colitis, a signature that includes the transcription of the key antimicrobial genes S100a8 and S100a9 (calprotectin). Genes involved in microbial resistance to oxidative stress, including Dps/ferritin, Fe-dependent peroxidase and glutathione S-transferase were identified as changing to a greater extent at the level of transcription than would be predicted by DNA abundance changes, implicating a role for increased oxygen tension and/or host-derived reactive oxygen species in driving transcriptional changes in commensal microbes.


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