Effect of cigarette smoking condensate on HDAC2 and inflammatory me-diators in mouse myoblast C2 C12 cells
10.3969/j.issn.1000-4718.2015.01.002
- VernacularTitle:香烟烟雾对 C2 C12小鼠成肌细胞 HDAC2及炎症介质的影响
- Author:
Dongmei HUANG
;
Zhiyi HE
;
Zhiying MA
;
Ying XIAO
- Publication Type:Journal Article
- Keywords:
Oxidative stress;
Histone deacetylase 2;
Muscular atrophy;
Chronic obstructive pulmonary disease
- From:
Chinese Journal of Pathophysiology
2015;(1):8-11
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the effect of cigarette smoking condensate on histone deacetylase 2 (HDAC2) and inflammatory mediators in mouse myoblast C 2C12 cells.METHODS:C2C12 cells were treated with cigarette smoke extract (CSE).HDAC2 siRNA was transfected into the cells using Lipofectamine TM 2000.The levels of interleukin-8 (IL-8) and tumor necrosis factor-α( TNF-α) in the culture supernatants were measured by ELISA , and the expression of HDAC2 at mRNA and protein levels was determined by real-time PCR and Western blotting .RESULTS:The expression of HDAC2 at mRNA and protein levels in CSE group was lower than that in control group (P<0.05).The supernatant levels of IL-8 and TNF-αin CSE group were significantly higher than those in control group ( P<0.05 ) .When the cells were transfected with HDAC2 siRNA followed by CSE stimulation , the expression of HDAC2 at mRNA and protein levels was de-creased , and the supernatant levels of IL-8 and TNF-αwere significantly increased as compared with CSE group and control group (P<0.05).CONCLUSION: Under the oxidative stress condition , C2C12 cells generate high levels of IL-8 and TNF-αby down-regulating the expression of HDAC2.
