A vitro experiment study of role of TLR4/NF-κB signal pathway in pathogenesis of brain injury during deep hypothermia circulatory arrest
10.3969/j.issn.1006-5725.2017.20.004
- VernacularTitle:TLR4/NF-κB信号通路在深低温停循环脑损伤发病机制中的体外实验研究
- Author:
Zhixian TANG
1
;
Zongren ZHONG
;
Ziyou LIU
;
Dan GUO
;
Liang XIONG
;
Zhiming DU
;
Chengnan TIAN
;
Zhenghong LAI
;
Chunfa XIE
;
Maolin ZHONG
Author Information
1. 赣南医学院第一附属医院
- Keywords:
TLR4;
NF-κB;
OGD/R;
BV2 microglia;
DHCA;
brain Injury
- From:
The Journal of Practical Medicine
2017;33(20):3344-3347
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of TLR4/NF-κB signal pathway in pathogenesis of brain inju-ry during deep hypothermia circulatory arrest(DHCA). Methods BV2 microglia cells were subjected to oxygen-glucose deprivation/reoxygenation(OGD/R),in vitro model for DHCA. The BV2 were randomly divided into the control group(C group)and the experimental group(O group). BV2 viability was determined by CCK-8 assay. TLR4 and its downstream signaling molecules ,MyD88 and phosphorylated NF-κB (p-p65) expressions were detected by Western blotting. TLR4 mRNA expression in BV2 microglial cells were determined by RT-PCR. Level of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in culture medium was detected by ELASA. Results Compared with the group C,BV2 microglia cell viability in experiment group was obviously weaker(P<0.05). Expressions of TLR4,MyD88 and phosphorylated NF-κB(p-p65)from the experiment group increased remarkedly than those from the group C (P < 0.05). TLR4 mRNA level was higher significantly in the group O than in the group C (P < 0.01). Production of IL-6 and TNF-α in the group O were up-regulated apparently compared to the group C(P<0.01). Conclusion TLR4/NF-κB signaling pathway contributed to activation of BV2 microglia cells treated by OGD/Reoxygenation ,which was probably the exactly way that involved in pathogenesis of brain injury during deep hypothermia circulatory arrest.
