Protective effect of esmolol on peritoneal macrophages in rats with sepsis
10.3760/cma.j.issn.1671-0282.2017.10.012
- VernacularTitle:艾司洛尔对脓毒症大鼠腹腔巨噬细胞保护作用的研究
- Author:
Xing LI
1
;
Zhongqian LU
;
Genhua MU
;
Yijun DENG
Author Information
1. 盐城市第一人民医院重症医学科
- Keywords:
Esmolol;
NF-κB;
β1-AR;
TNF-α
- From:
Chinese Journal of Emergency Medicine
2017;26(10):1155-1159
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effects of esmolol on peritoneal macrophages in rats with sepsis.Methods Rat peritoneal macrophages were deprived of serum and divided into four groups,namely normal group,LPS stimulated group,esmolol group and LPS plus esmolol group.Quantitative real-time PCR and Western blot were performed to assay the expressions and protein levels of TNF-α,β1-AR and p65.The activation of NF-κB was determined by electrophoretic mobility shift assay.Results The expression of TNF-α mRNA and protein level was significantly increased in LPS-treated group than those in normal group (P ＜ 0.01),and those in LPS plus esmolol group was significantly lower than those in LPS stimulated group (P ＜ 0.01).The expression of β1-AR mRNA and protein level were significantly higher in LPS-treated group than those in normal group (P ＜ 0.01),The expression of β1-AR mRNA and protein level in the esmolol group was lower than those in normal group (P ＜ 0.01),and those in LPS plus esmolol group was lower than those in LPS stimulated group (P ＜ 0.01).Besides,compared with the normal group,the expression of p65 mRNA in the LPS stimulated group was noticeably higher (P ＜ 0.01).The expression of P65 mRNA in LPS plus esmolol group was significantly lower than that in LPS-treated group (P ＜ 0.01).The NF-κB/DNA binding force in the LPS stimulated group was significantly higher than that in normal group (P ＜0.01).Compared with the LPS stimulated group,the NF-κB/DNA binding force in the LPS plus esmolol group was significantly lower (P ＜ 0.01).Conclusions The expression of TNF-α mRNA induced by LPS was decreased by esmolol in rat peritoneal macrophages which might be achieved via inhibiting NF-κB pathway by the modulation role of β1 adrenergic receptor.
