Effect of STAT3 down-regulation on airway injury in asthma
10.3969/j.issn.1000-4718.2017.12.025
- VernacularTitle:干扰STAT3基因对哮喘气道损伤的影响
- Author:
jian Yuan YANG
1
;
Zhen ZHANG
;
Zhe CHENG
Author Information
1. 郑州大学第一附属医院呼吸与危重症医学科
- Keywords:
Signal transducer and activator of transcription 3;
Asthma;
Bronchial epithelial cells;
Inflamma-tory cytokines;
Oxidative stress
- From:
Chinese Journal of Pathophysiology
2017;33(12):2269-2273
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the effect of signal transducer and activator of transcription 3 (STAT3) on air-way injury in asthma and its mechanism .METHODS:The expression and activation of STAT 3 in bronchial mucosa tissues of asthmatic patients were measured by Western blot .The expression and activation of STAT 3 in bronchial epithelial cells pretreated with Dermatophagoides pteronyssinus antigen P1 (Derp1) were estimated.Bronchial epithelial cells were trans-fected with STAT3 shRNA.STAT3 expression was measured by Western blot .The cell viability was detected by CCK-8 as-say.The concentrations of TNF-α, IL-1βand IL-6 were detected by ELISA .The content of malondialdehyde ( MDA) and the activity of superoxide dismutase ( SOD) and glutathione peroxidase ( GSH-Px) were also determined for evaluating the status of oxidative stress .The cell apoptosis was analyzed by flow cytometry .RESULTS:The protein level of p-STAT3 was significantly up-regulated in both bronchial mucosa of asthmatic tissues and bronchial epithelial cells pretreated with Derp 1. Knockdown of STAT3 inhibited the releases of TNF-α, IL-1βand IL-6, decreased the content of MDA and enhanced the activity of SOD and GSH-Px with the suppression of cell apoptosis ( P <0.05 ) .CONCLUSION: Down-regulation of STAT3 attenuates Derp1-induced the airway injury .The mechanism may involve that knockdown of STAT3 suppresses the activation of JAK/STAT signaling pathway , the release of asthma-related inflammatory cytokines and oxidative stress in bronchial epithelial cells , thus inhibiting cell apoptosis .
