Effect of Gas6 in silica-induced inflammation on differentiated human acute monocytic leukemia (THP-1) macrophages
10.3760/cma.j.issn.1001-9391.2017.01.001
- VernacularTitle: Gas6抑制石英粉尘导致的巨噬细胞炎性反应
- Author:
Yan SHEN
1
;
Xiuqing CUI
;
Yi RONG
;
Min ZHOU
;
Lili XIAO
;
Wei LI
;
Zhihong ZHANG
;
Weihong CHEN
Author Information
1. Department of Occupational an Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
- Publication Type:Journal Article
- Keywords:
Gas6;
Quartz;
Macrophage
- From:
Chinese Journal of Industrial Hygiene and Occupational Diseases
2017;35(1):1-6
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the modulation role of Gas6 in silica-induced inflammatory effect on human macrophages.
Methods:Differentiated THP-1 macrophages were exposed to different concentrations of silica for 6 h and 24 h. Additionally, silica-activated macrophages were treated with different concentrations of recombine human Gas6 and Gas6 antibody respectively. Cell viabilities were determined by CCK-8 kit. Expression levels of Gas6 and inflammatory cytokines (TNF-α, IL-1β and IL-6) were measured by ELISA assay kits.
Results:Silica particles induced clear dose-dependent decreases of cell viability and Gas6 expression at both 6 h and 24 h. The cell viability of 24 h is lower than 6 h at the same concentration of silica (P<0.05). Furthermore, silica activated macrophages treated with Gas6 antibody induced significant decreases of Gas6 both at 6 h and 24 h (P<0.05). After pretreated with various concentrations of Gas6 antibody, silica induced higher expressions of inflammatory cytokines (TNF-α, IL-1β, IL-6) in dose-dependent manners at two time points. Addition of exoge-nous Gas6 significantly suppressed silica-induced inflammatory cytokines concentrations mentioned above in the cell culture supernatants in clear dose-dependent manners.
Conclusion:Exogenous Gas6 could inhibit the secre-tion of inflammatory cytokines in macrophages, while the block of Gas6 might enhance this inflammation.
