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雌二醇可预防雄性大鼠肠道缺血再灌注引起的肠道通透性和蠕动变化。

Estradiol prevented intestinal ischemia and reperfusion-induced changes in intestinal permeability and motility in male rats.

作者信息

Ricardo-da-Silva Fernanda Yamamoto, Fantozzi Evelyn Thaís, Rodrigues-Garbin Sara, Domingos Helori Vanni, Oliveira-Filho Ricardo Martins, Vargaftig Bernardo Boris, Riffo-Vasquez Yanira, Breithaupt-Faloppa Ana Cristina, Tavares-de-Lima Wothan

机构信息

Laboratorio de Cirurgia Cardiovascular e Fisiopatologia da Circulacao (LIM-11), Instituto do Coracao (InCor), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, BR.

Departamento de Farmacologia, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo, SP, BR.

出版信息

Clinics (Sao Paulo). 2021 Apr 26;76:e2683. doi: 10.6061/clinics/2021/e2683. eCollection 2021.

DOI:10.6061/clinics/2021/e2683
PMID:33909827
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8050597/
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.

摘要

目的

肠道缺血再灌注（I/R）可导致严重的内皮损伤，损害肠道蠕动。据报道，雌二醇可控制I/R损伤诱导的局部和全身炎症。因此，我们研究了雌二醇治疗对肠道I/R模型局部影响的作用。

方法

通过肠系膜上动脉闭塞（45分钟）使大鼠遭受缺血，随后进行再灌注（2小时）。在缺血诱导后30分钟（E30），给予单剂量17β-雌二醇（E2，280μg/kg，静脉注射）。假手术动物用作对照。

结果

I/R损伤降低了肠道蠕动，增加了肠道通透性，同时肠系膜内皮型一氧化氮合酶（eNOS）和内皮素（ET）蛋白表达降低。此外，血清损伤标志物和炎症介质水平升高。雌二醇治疗改善了肠道蠕动，降低了肠道通透性，并增加了eNOS和ET表达。雌二醇治疗后损伤标志物和炎症介质水平也降低。

结论

总体而言，我们的研究结果表明，雌二醇治疗可调节I/R损伤对肠道的有害影响。因此，雌二醇介导肠道屏障功能的改善并预防肠道功能障碍，这可能会减轻全身炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b70c/8050597/c18aeafdbba4/cln-76-e2683-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b70c/8050597/f1b92ba450a4/cln-76-e2683-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b70c/8050597/ed6dfc7eea4f/cln-76-e2683-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b70c/8050597/675970f5abed/cln-76-e2683-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b70c/8050597/653e9cc20618/cln-76-e2683-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b70c/8050597/c83834120ac7/cln-76-e2683-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b70c/8050597/c18aeafdbba4/cln-76-e2683-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b70c/8050597/f1b92ba450a4/cln-76-e2683-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b70c/8050597/ed6dfc7eea4f/cln-76-e2683-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b70c/8050597/675970f5abed/cln-76-e2683-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b70c/8050597/653e9cc20618/cln-76-e2683-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b70c/8050597/c83834120ac7/cln-76-e2683-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b70c/8050597/c18aeafdbba4/cln-76-e2683-g006.jpg

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