BPA disrupts 17-estradiol-mediated hepatic protection against ischemia/reperfusion injury in rat liver by upregulating the Ang II/AT1R signaling pathway

Autor: Zeyu Li, Yili Zhang, Yu Shi, Mei Zhang, Liang Yu, Liankang Sun, Sheng-Li Wu
Jazyk: angličtina
Rok vydání: 2020
Předmět:
0301 basic medicine
Male
Cancer Research
bisphenol A
Endocrine Disruptors
Biochemistry
Rats
Sprague-Dawley

chemistry.chemical_compound
0302 clinical medicine
estrogen
rat
biology
Estradiol
Chemistry
Angiotensin II
Articles
Up-Regulation
Losartan
Xenoestrogen
Oncology
Endocrine disruptor
Liver
030220 oncology & carcinogenesis
Reperfusion Injury
Molecular Medicine
Alkaline phosphatase
hormones
hormone substitutes
and hormone antagonists

medicine.drug
Signal Transduction
medicine.medical_specialty
endocrine system
ischemia-reperfusion injury
Protective Agents
Receptor
Angiotensin
Type 1

03 medical and health sciences
Phenols
Internal medicine
Genetics
medicine
Animals
Benzhydryl Compounds
Molecular Biology
urogenital system
Estrogens
medicine.disease
Rats
030104 developmental biology
Endocrinology
Alanine transaminase
biology.protein
Liver function
Reperfusion injury
Zdroj: Molecular Medicine Reports
ISSN: 1791-3004
1791-2997
Popis: Bisphenol A (BPA), a xenoestrogen commonly used in plastics, may act as an endocrine disruptor, which indicates that BPA might be a public health risk. The present study aimed to investigate the effect of BPA on 17β‑estradiol (E2)‑mediated protection against liver ischemia/reperfusion (I/R) injury, and to identify the underlying mechanisms using a rat model. A total of 56 male Sprague Dawley rats were randomly divided into the following seven groups: i) Sham; ii) I/R; iii) Sham + BPA; iv) I/R + BPA; v) I/R + E2; vi) I/R + E2 + BPA; and vii) I/R + E2 + BPA + losartan [LOS; an angiotensin II (Ang II) type I receptor (ATIR) antagonist]. A rat model of hepatic I/R injury was established by inducing hepatic ischemia for 60 min followed by reperfusion for 24 h. When ischemia was induced, rats were treated with vehicle, E2, BPA or LOS. After 24 h of reperfusion, blood samples and hepatic tissues were collected for histopathological and biochemical examinations. The results suggested that 4 mg/kg BPA did not significantly alter the liver function, or Ang II and AT1R expression levels in the Sham and I/R groups. However, 4 mg/kg BPA inhibited E2‑mediated hepatic protection by enhancing hepatic necrosis, and increasing the release of alanine transaminase, alkaline phosphatase and total bilirubin (P
Databáze: OpenAIRE
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