English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

BRANCO, L. T. P. Oxidative and Neurogenic Mechanisms of Bowel Inflammation in an Experimental Model of Gastroschisis. 85 p. Thesis (Master in Pharmacology) – Institute of Biomedical Sciences, University of São Paulo, São Paulo, 2008 Gastroschisis (G) is a congenital defect of the abdominal wall closure resulting in perivisceritis due to contact between the bowel and amniotic fluid. This study was undertaken to evaluate the involvement of neurovascular and oxidative mechanisms in this condition by analyzing the gene and proteic expressions of neurogenic and oxidative markers in the gut of foetus with G from female rats treated with dexamethasone or its vehicle saline. A marked increase of myeloperoxidase (MPO) activity was observed in the gut of foetus with G in comparison to control (C), but not sham (S), group. Groups with G exposed to dexamethasone exhibited the same MPO values as compared to CT. However, this treatment caused a significant reduction of MPO activity in sham-treated group (ST). The mRNA expression of NK2 receptor (preferential for NKA) in both G and S groups was significantly reduced in the gut of these animals compared to C group. Neither NK1 receptor (preferential for substance P) nor both vasoactive intestinal peptide receptors type 1 and 2 (VIP) and TRPV1 receptor mRNA expression was different between G and control groups (C and S). Treatment with dexamethasone reversed the reduced expression of NK2 in the gut of foetus with GT and ST, but significantly increased the mRNA expression of NK1 receptor. Increased mRNA expression of iNOS, but not nNOS and eNOS, was observed in G group when compared to S group. Dexamethasone treatment evoked a further increase in the mRNA expression of eNOS, nNOs and iNOS as compared to G group without treatment. The induction of G produced a significant increase in the mRNA expression of cyclooxygenase type 2 (COX-2), but not COX-1, and dexamethasone treatment did not interfere in these responses. Western blot analysis showed that neither SOD-1 nor protein nitration was different among groups with G and control. However, a significant increase of protein nitration was observed in G group treated with dexamethasone. Elevated concentrations of interleukin 6 (IL-6), but not TNF-α and IL-1β, was found in the intestine of foetus with G when compared to C group. The increase was not affected by dexamethasone. In conclusion, it is likely that the inflammatory process observed in the gut of foetus with gastroschisis arises through a combination of neurogenic mechanisms that act in concert with reactive oxygen species and possible generation of prostanoids via COX-2 to produce gut dysfunction. This data may have a major impact in developing strategies and markers to recognize gut impairment in the event of gastroschisis.

Investigação farmacológica de mecanismos neurogênicos e oxidativos no modelo experimental de gastrosquise em ratos.