Estradiol prevented intestinal ischemia and reperfusion-induced changes in intestinal permeability and motility in male rats
Clinics
;
76: e2683, 2021. graf
Article
Dans Anglais
| LILACS
| ID: biblio-1249591
ABSTRACT
OBJECTIVES:
Ischemia and reperfusion (I/R) in the intestine could lead to severe endothelial injury, compromising intestinal motility. Reportedly, estradiol can control local and systemic inflammation induced by I/R injury. Thus, we investigated the effects of estradiol treatment on local repercussions in an intestinal I/R model.METHODS:
Rats were subjected to ischemia via the occlusion of the superior mesenteric artery (45 min) followed by reperfusion (2h). Thirty minutes after ischemia induction (E30), 17β-estradiol (E2) was administered as a single dose (280 μg/kg, intravenous). Sham-operated animals were used as controls.RESULTS:
I/R injury decreased intestinal motility and increased intestinal permeability, accompanied by reduced mesenteric endothelial nitric oxide synthase (eNOS) and endothelin (ET) protein expression. Additionally, the levels of serum injury markers and inflammatory mediators were elevated. Estradiol treatment improved intestinal motility, reduced intestinal permeability, and increased eNOS and ET expression. Levels of injury markers and inflammatory mediators were also reduced following estradiol treatment.CONCLUSION:
Collectively, our findings indicate that estradiol treatment can modulate the deleterious intestinal effects of I/R injury. Thus, estradiol mediates the improvement in gut barrier functions and prevents intestinal dysfunction, which may reduce the systemic inflammatory response.
Texte intégral:
Disponible
Indice:
LILAS (Amériques)
Sujet Principal:
Lésion d'ischémie-reperfusion
/
Oestradiol
Type d'étude:
Étude pronostique
Limites du sujet:
Animaux
langue:
Anglais
Texte intégral:
Clinics
Thème du journal:
Médicament
Année:
2021
Type:
Article
Pays d'affiliation:
Brésil
/
Royaume-Uni
Institution/Pays d'affiliation:
Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo/BR
/
Instituto de Ciencias Biomedicas, Universidade de Sao Paulo/BR
/
Kings College London/GB
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