A vitro experiment study of role of TLR4/NF-κB signal pathway in pathogenesis of brain injury during deep hypothermia circulatory arrest
TANG Zhixian
ZHONG Zongren
LIU Ziyou
GUO Dan
XIONG Liang
DU Zhiming
TIAN Chengnan
LAI Zhenghong
XIE Chunfa
ZHONG Maolin
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.
Keywords：TLR4NF-κBOGD/RBV2 microgliaDHCAbrain Injury
Publication Date：2017-10-16
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：4( 3344-3347 )