| First Author | Sun HN | Year | 2018 |
| Journal | Mol Med Rep | Volume | 18 |
| Issue | 2 | Pages | 2427-2432 |
| PubMed ID | 29901182 | Mgi Jnum | J:294795 |
| Mgi Id | MGI:6458611 | Doi | 10.3892/mmr.2018.9170 |
| Citation | Sun HN, et al. (2018) Peroxiredoxin I deficiency increases LPSinduced lethal shock in mice. Mol Med Rep 18(2):2427-2432 |
| abstractText | Peroxiredoxin I (Prx I) plays a role in regulating macrophage proinflammatory cytokine production and gene expression and participates in immune regulation. However, the possible protective role of Prx I in endotoxininduced lethal shock is poorly understood. In the present study, western blot analysis, ELISA and haematoxylin and eosin staining were performed to examine the protein expression of cytoines and analyses the levels of cytokines in the serum and tissue to evaluate the tissue damage. The present study revealed that lipopolysaccharide (LPS)induced lethality in Prx I/ mice was is accelerated via the observed decreased serum IL10 levels. Results also demonstrated rapid immune cell infiltration and oxidative stress in the Prx I/mice liver after LPS injections. These phenomena increased liver apoptosis through increasing cleaved caspase3 protein expression in Prx I/ mice after LPS injections, resulting in high lethality after LPS challenges. These findings provide a new insight for understanding the function of Prx I against endotoxininduced injury. |
