College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, Heilongjiang 163319, P.R. China.
Laboratory Animal Center, Dalian Medical University, Dalian, Liaoning 116044, P.R. China.
Mol Med Rep. 2018 Aug;18(2):2427-2432. doi: 10.3892/mmr.2018.9170. Epub 2018 Jun 14.
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 endotoxin‑induced 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 IL‑10 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 caspase‑3 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 endotoxin‑induced injury.
过氧化物酶 I（Prx I）在调节巨噬细胞前炎性细胞因子的产生和基因表达以及参与免疫调节中发挥作用。然而，Prx I 在内毒素诱导的致死性休克中可能具有的保护作用仍知之甚少。在本研究中，通过蛋白质印迹分析、酶联免疫吸附试验和苏木精和伊红染色，检测细胞因子的蛋白表达，并分析血清和组织中细胞因子的水平，以评估组织损伤。本研究表明，通过观察到血清 IL-10 水平降低，Prx I-/- 小鼠中脂多糖（LPS）诱导的致死性作用被加速。结果还表明，LPS 注射后，Prx I-/- 小鼠肝脏中出现快速的免疫细胞浸润和氧化应激。这些现象通过增加 LPS 注射后 Prx I-/- 小鼠中 cleaved caspase-3 蛋白的表达，增加了肝细胞凋亡，导致 LPS 挑战后的高死亡率。这些发现为理解 Prx I 对抗内毒素诱导损伤的功能提供了新的见解。
