Silencing of peroxiredoxin 1 expression ameliorates ulcerative colitis in a rat model

Background Peroxiredoxin 1 (PRDX1), a protein with anti-inflammatory and anti-apoptotic properties, shows elevated expression in ulcerative colitis (UC). However, PRDX1's specific role in UC is poorly understood. Methods UC was induced in rats using dextran sulfate sodium (DSS). In vivo RNA int...

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Veröffentlicht in:Journal of international medical research 2021-03, Vol.49 (3), p.300060520986313-300060520986313
Hauptverfasser: Wu, Na, Du, Xinchong, Peng, Zhao, Zhang, Zetian, Cui, Lijun, Li, Duo, Wang, Rui, Ma, Maoyuan
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Sprache:eng
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Zusammenfassung:Background Peroxiredoxin 1 (PRDX1), a protein with anti-inflammatory and anti-apoptotic properties, shows elevated expression in ulcerative colitis (UC). However, PRDX1's specific role in UC is poorly understood. Methods UC was induced in rats using dextran sulfate sodium (DSS). In vivo RNA interference was used to silence the PRDX1 expression. PRDX1 expression levels and the inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, transforming growth factor (TGF)-β and interferon (IFN)-γ in tissues were assessed by real-time quantitative polymerase chain reaction and western blotting. Colonic injury was assessed by hematoxylin–eosin staining. ELISA was used to assess levels of the inflammatory cytokines TNF-α, IL-1β and IL-6 in colon tissues. Apoptosis of intestinal epithelial cells was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling, and expression of the apoptotic proteins bcl-2, Bax, cleaved caspase-3 and caspase-3 was assessed by western blotting. Results PRDX1 expression was significantly increased in rats with DSS-induced UC. Silencing of PRDX1 expression improved colon injury in rats with DSS-induced UC. In addition, silencing of PRDX1 expression inhibited inflammatory responses and apoptosis of intestinal epithelial cells in rats with DSS-induced UC. Conclusions Silencing of PRDX1 expression can ameliorate colon injury in rats with DSS-induced UC.
ISSN:0300-0605
1473-2300
DOI:10.1177/0300060520986313