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 |
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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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