Related Experiment Video
Updated: Aug 29, 2026
The Chick Chorioallantoic Membrane In Vivo Model to Assess Perineural Invasion in Head and Neck Cancer
Published on: June 21, 2019
Local dexamethasone improves the intestinal lesions of gastroschisis in chick embryos
Jiakang Yu1, Salome Gonzalez-Reyes, Juan A Diez-Pardo
1Research Laboratory, Hospital Infantil Universitario La Paz, P. de la Castellana 261, 28046 Madrid, Spain.
Insights
Dexamethasone treatment improved bowel health in gastroschisis (Gx) chick embryos. It reduced wall thickening and normalized DNA and neural density in the eviscerated bowel.
Area of Science:
- Developmental biology
- Gastroenterology
- Pharmacology
Background:
- Gastroschisis (Gx) in embryos causes eviscerated bowel with functional deficits.
- Parietal lesions in Gx require effective management strategies.
Purpose of the Study:
- To investigate the potential benefits of dexamethasone on parietal lesions in Gx chick embryos.
- To test if dexamethasone exposure can mitigate Gx-induced bowel abnormalities.
Main Methods:
- Gastroschisis (Gx) was surgically induced in chick embryos.
- Dexamethasone or saline was administered via the amnio-allantoic chamber.
- Intestinal tissues were analyzed for thickness, DNA, protein, and neural density.
Main Results:
- Gx embryos exhibited reduced body weight, tibial length, and intestinal DNA, with thickened bowel walls and decreased neural density.
- Dexamethasone treatment normalized body weight, tibial length, intestinal DNA, and neural density.
- Dexamethasone partially improved intestinal wall thickness and serosal width.
Conclusions:
- Local dexamethasone administration shows beneficial effects on the eviscerated bowel in Gx.
- Dexamethasone treatment can decrease wall thickening, normalize DNA, and increase neural populations in Gx bowels.
- Late gestational steroid exposure may be a viable strategy for preventing intestinal lesions in Gx.
Background And Aims:
Eviscerated bowel in gastroschisis (Gx) undergoes changes that lead to dysfunctions and create management difficulties. This study tests the hypothesis that exposure of the eviscerated bowel of chick embryos with Gx to dexamethasone might have beneficial effects on the parietal lesions.
Methods:
Gx was created in chick embryos on incubation day 15 and either dexamethasone (0.047 mg in 0.24 ml) or 0.075% saline were instilled into the amnio-allantoic chamber on day 17. The chicks were recovered near hatching (day 19) and eviscerated and non-eviscerated portions of the intestines were recovered, weighed and processed for HE and synaptophysin staining or for total DNA and protein measurements. Total mural and serosal layer thickness were determined and intramural ganglia were counted. ANOVA was used for comparison among groups with significance level set at p<0.05.
Results:
Chicks with Gx and Gx + saline controls had reduced body weight and tibial length in comparison with controls. The eviscerated bowel was heavier with marked wall thickening at the expense of all layers but particularly of the serosa. They had decreased total intestinal DNA with normal protein and decreased intramural ganglion density. In contrast, chicks from the Gx + dexamethasone group had normal body weight and tibial length, near-normal intestinal wall thickness with slightly increased serosal width, near-normal intestinal DNA content and normal density of intramural ganglia.
Conclusion:
Local dexamethasone had beneficial effects on the eviscerated bowel of chicks with Gx as judged by decreased wall thickening, normalization of total intestinal DNA and richer neural population. Late gestational exposure to steroids could represent another alternative for preventing intestinal lesions in Gx.
