Effect of recombinant rat CC16 protein on LPS-induced expression of TNF-α, IL-6 and IL-8 in rat tracheal epithelial cells
10.3969/j.issn.1000-4718.2016.10.017
- VernacularTitle:重组大鼠CC16蛋白质对LPS诱导大鼠气道上皮细胞表达TNF-α、IL-6和IL-8的影响
- Author:
Min PANG
;
Dong WANG
;
Ting LI
;
Dan WANG
;
Lirong YUAN
;
Min GUO
;
Hailong WANG
- Publication Type:Journal Article
- Keywords:
CC16 protein;
Airway inflammation;
LPS;
Inflammatory mediators;
Nuclear factor-κB
- From:
Chinese Journal of Pathophysiology
2016;32(10):1843-1847
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To explore the effect of recombinamt rat CC16 protein (rCC16) on LPS-induced expression of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and IL-8 in the rat tracheal epithelial (RTE) cells. METHODS:The RTE cells were incubated with rCC16 at concentrations of 0.5, 1.0 and 2.0 mg/L in serum-free media for 2 h prior to LPS (0.1 mg/L) treatment for further 24 h.The cells were harvested for assessing the mRNA levels of TNF-α, IL-6 and IL-8 by RT-qPCR.The cell culture supernatants were collected for analyzing the protein levels of TNF -α, IL-6 and IL-8 by ELISA.In addition, the nuclear translocation of nuclear factor-κB (NF-κB) p65 was tested by Western blot.RESULTS:rCC16 inhibited LPS-induced IL-6 and IL-8 expression at both mRNA and protein levels in the RTE cells in a concentration-dependent (0~2 mg/L) manner, as demonstrated by RT-qPCR and ELISA.However, no concentra-tion-dependent manner between the dose of rCC 16 and TNF-αexpression was observed , and rCC16 inhibited LPS-induced TNF-αexpression at lower concentration (0.5 mg/L).rCC16 concentration-dependently inhibited the effects of LPS on the level of nuclear translocation of NF-κB p65.CONCLUSION:rCC16 suppresses LPS-mediated TNF-α, IL-6 and IL-8 pro-duction through inactivation of NF-κB activity in RTE cells .
