[C1q and tumor necrosis factor related protein 4 (CTRP4) suppresses caspase-1/IL-1ß inflammatory pathway in trophoblasts of rat models with preeclampsia].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
; 32(11): 1441-1445, 2016 Nov.
Article
em Zh
| MEDLINE
| ID: mdl-27774931
Objective To explore the effect of C1q/tumor necrosis factor related protein 4 (CTRP4) on the placental trophoblasts of preeclampsia model rats. Methods Placental trophoblastic tissues were respectively collected from normal pregnant rats and model rats with preeclampsia, and then mRNA and protein expression levels of CTRP4, interleukin 1ß (IL-1ß), and caspase-1 were detected with quantitative real-time PCR (qRT-PCR) and Western blotting. Primary placental trophoblasts were isolated from normal pregnant rats and model rats; at different time points, flow cytometry was used to detect the number of PI+caspase-1+ pyroptotic cells; and qRT-PCR and Western blotting were used to detect expression levels of IL-1ß and caspase-1. Finally, recombinant CTRP4 protein (at the doses of 0.5, 5, 15, 25 or 50 ng/mL) or neutralizing CTRP4 antibody (at the doses of 10 or 20 ng/mL) were added into the medium of trophoblasts from model rats; after incubation for 72 h, the number of pyroptotic cells and the expression levels of IL-1ß and caspase-1 were detected. ResultsCaspase-1/IL-1ß inflammatory pathway was activated and CTRP4 expression was downregulated in placenta trophoblastic tissue from rats with preeclampsia. CTRP4 recombinant protein treatment significantly inhibited pyroptosis and the caspase-1/IL-1ß pathway in trophoblasts derived from rats with preeclampsia, while CTRP4 neutralizing antibody treatment had an opposite effect on pyroptosis and inflammation. Conclusion CTRP4 can significantly inhibit the activation of caspase-1/IL-1ß inflammatory pathway, and suppress the pyroptosis of trophoblasts derived from rats with preeclampsia.
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Base de dados:
MEDLINE
Assunto principal:
Pré-Eclâmpsia
/
Trofoblastos
/
Citocinas
/
Caspase 1
/
Interleucina-1beta
Idioma:
Zh
Ano de publicação:
2016
Tipo de documento:
Article