THE ROLE OF SEX HORMONES IN THE INTESTINAL INJURY AFTER BRAIN DEATH USING A SURGICAL MENOPAUSE MODEL IN RATS.

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Tác giả: Ana Cristina Breithaupt-Faloppa, Cristiano de Jesus Correia, Elizabeth Cristina Miola, Luiz Felipe Pinho Moreira, Fernanda Yamamoto Ricardo-da-Silva, Marina Vidal-Dos-Santos, Pedro Luiz Zonta de Freitas

Ngôn ngữ: eng

Ký hiệu phân loại: 972.8202 *Central America

Thông tin xuất bản: Ireland : Molecular and cellular endocrinology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 165107

 Among transplantable organs, the intestine is one of the most challenging organs to transplant. While there is considerable research on the effects of brain death (BD), little is known about the specific intestinal changes that occur, particularly in females. Here we investigated the role of female sex hormones in the BD-induced intestinal inflammation, using an ovariectomy (OVx) model for sex hormones depletion. Wistar rats (female) were divided into four experimental groups: Control non-OVx - non-manipulated
  Control-OVx -ovariectomized
  BD non-OVx - animals submitted to BD (6h)
  BD-OVx -ovariectomized animals submitted to BD. OVx was performed 10 days before BD induction. non-OVx groups were chosen during proestrus phase (heat period). Inflammatory mediators and white blood cell count were quantified in the blood. Intestine tissue was sampled for histopathological analysis, myeloperoxidase (MPO) activity, Evans blue dye extravasation assay and immunohistochemistry. Results show higher intestinal injury in BD-OVx than BD non-OVx animals, presenting reduced crypt depth and increased serum inflammatory mediators. Independently from the previous hormonal status, BD increased intestinal inflammation, with higher leukocyte infiltration, MPO activity, ICAM-1 expression, and higher serum MIP-1α. In summary, BD modulates intestinal inflammation by increasing leukocyte mobilization. Whereas OVx, and its consequences on the female hormonal profile, influences homeostasis and BD-induced inflammation, increasing inflammatory mediators and altering intestinal morphology.
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