Publication: Evaluation of HIF-1α and iNOS in ischemia/reperfusion gastric model: bioimpedance, histological and immunohistochemical analyses
Authors
Peña Mercado, Eduardo ; Garcia Lorenzana, Mario ; Arechaga Ocampo, Elena ; González De la Rosa, Claudia H. ; Beltran, Nohra E.
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Publisher
Universidad de Murcia. Departamento de Biología Celular e Histología
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DOI
DOI: 10.14670/HH-11-975
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info:eu-repo/semantics/article
Description
Abstract
Gastrointestinal ischemia/reperfusion (I/R)
generates pathological alterations that could lead to
death. Early ischemic damage markers could be used to
guide therapy and improve outcomes. Aim. To relate
hypoxia-inducible factor 1α (HIF-1α) activation and
inducible nitric oxide synthase (iNOS) expression to
gastric impedance changes due to I/R damage. Methods.
Experimental animals were randomly distributed into 3
groups: control, ischemia (30 min) and I/R (60 min).
Gastric ischemia was generated by celiac artery
clamping for 30 min, and then blood flow was restored
for 60 min. Impedance spectra and biopsies of the
glandular portion were obtained for histological and
immunohistochemical analyses. Immunodetection of
both HIF-1α and iNOS was performed. Results. Under
ischemia and I/R conditions, there was an increase
(p<0.05) in the impedance parameters. Histologically,
under ischemic conditions, edema and necrosis were
observed in epithelium and significant vascular
congestion. In I/R condition, alterations of the glandular
and luminal integrity were found, which generated areas
of epithelial erosion. Immunohistochemical analysis of
HIF-1α revealed an increase (p<0.01) in the number of
immunoreactive cells in the ischemia (35.7±13.9) and
I/R (119.9±18.8) conditions compared to the control
(0.8±1.2). Immunodetection of iNOS showed an
increase (p<0.01) in the number of cells expressing
iNOS under the ischemia (5.4±2.9) and I/R conditions
(27.4±11.3) was observed compared to the control
(0.4±0.8). Conclusion. Early changes in impedance in
response to I/R is related to histopathological changes,
the nuclear stabilization and translocation of HIF-1α as
well as expression of iNOS.
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Citation
Histology and Histopathology, Vol.33, nº8, (2018)
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