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Selenium attenuates the cadmium-induced placenta glucocorticoid barrier damage by up-regulating the expression of specificity protein 1.

Abstract
Cadmium (Cd) is an environmental pollutant and pregnant women are especially susceptible to the effects of exposure to Cd. Our previous study found Cd can be accumulated in the placenta and causes fetal growth restriction (FGR) through damage the placental glucocorticoid barrier. Selenium (Se), as an essential micronutrient, can allivate Cd-induced toxicity. In this study, we aim to explore the protective mechanism of Se against Cd-induced the placental glucocorticoid barrier damage and FGR. Pregnant Sprague Dawley (SD) rats were exposed to CdCl2 (1 mg/kg/day) and Na2 SeO3 (0.1-0.2-0.3 mg/kg/day) by gavage from gestational day (GD) 0 to GD 19. The results showed that reduced fetal weight, increased corticosterone concentrations in the maternal and fetal serum, and impaired placental labyrinth layer blood vessel development, appeared in pregnant rats after Cd exposure and improved after treated with Se. In cell experiments, we confirmed that Se reduces Cd-induced apoptosis. Moreover, Se can abolish Cd-induced 11β-HSD2 and specificity protein 1 (Sp1) decreasing in vivo and vitro. In human JEG-3 cells, the knockdown of Sp1 expression by small interfering RNA can suppressed the protective effect of Se on Cd-induced 11β-HSD2 decreasing. In general, our results demonstrated that Se is resistant to Cd-induced FGR through upregulating the placenta barrier via activation of the transcription factor Sp1.
AuthorsSisi Wu, Na Chen, Xia Tong, Xu Xu, Qihui Chen, Fan Wang
JournalJournal of biochemical and molecular toxicology (J Biochem Mol Toxicol) Vol. 36 Issue 7 Pg. e23056 (Jul 2022) ISSN: 1099-0461 [Electronic] United States
PMID35384129 (Publication Type: Journal Article)
Copyright© 2022 Wiley Periodicals LLC.
Chemical References
  • Glucocorticoids
  • Sp1 Transcription Factor
  • SP1 protein, human
  • Cadmium
  • 11-beta-Hydroxysteroid Dehydrogenase Type 2
  • Selenium
Topics
  • 11-beta-Hydroxysteroid Dehydrogenase Type 2 (genetics, metabolism, pharmacology)
  • Animals
  • Cadmium (toxicity)
  • Cadmium Poisoning (metabolism)
  • Cell Line, Tumor
  • Female
  • Fetal Growth Retardation (chemically induced, metabolism)
  • Glucocorticoids (pharmacology)
  • Humans
  • Placenta (metabolism)
  • Pregnancy
  • Rats
  • Rats, Sprague-Dawley
  • Selenium (adverse effects)
  • Sp1 Transcription Factor (biosynthesis)

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