Mechanism of TLR-4/NF-κB pathway in myocardial ischemia reperfusion injury of mouse

Hao Chen; Ruo-Qing Zhang; Xiao-Gang Wei; Xiao-Min Ren; Xiao-Qian Gao

doi:10.1016/j.apjtm.2016.03.021

Mechanism of TLR-4/NF-κB pathway in myocardial ischemia reperfusion injury of mouse

Asian Pac J Trop Med. 2016 May;9(5):503-7. doi: 10.1016/j.apjtm.2016.03.021. Epub 2016 Mar 23.

Authors

Hao Chen¹, Ruo-Qing Zhang², Xiao-Gang Wei², Xiao-Min Ren², Xiao-Qian Gao³

Affiliations

¹ Department of Cardiology, Affiliated People's Hospital of Hebei Medical University, Hebei 050000, China; Shijiazhuang No.1 Hospital, Shijiazhuang, Hebei 050000, China. Electronic address: hbch1120@163.com.
² Department of Cardiology, Affiliated People's Hospital of Hebei Medical University, Hebei 050000, China; Shijiazhuang No.1 Hospital, Shijiazhuang, Hebei 050000, China.
³ Department of Internal Medicine, Zhengding Hospital, Zhengding, Hebei 050000, China.

PMID: 27261863
DOI: 10.1016/j.apjtm.2016.03.021

Abstract

Objective: To detect the expression of Toll-like receptor 4 (TLR-4) and NF-κB and to discuss the mechanism of TLR-4/NF-κB pathway in the myocardial ischemia reperfusion injury of mouse.

Methods: TLR-4 mutant mice and wild homozygous mice were divided into the model group and sham group. Mice in the model group were given the ligation of left anterior descending coronary artery for the modeling, while mice in the sham group were not given the ligation after threading. The cardiac muscle tissues were collected for the morphological observation. The immunohistochemistry was employed to detect the expression of NF-κB, Western blot was used to detect the expression of TLR-4 and ELISA to detect the expression of serum inflammatory factors.

Results: The expression of NF-κB in TLR-4 null mice after the myocardial ischemia reperfusion was significantly lower than that in wild homozygous mice. For the model group and sham group, the expression of TLR-4 in wild homozygous mice was all significantly higher than that in TLR-4 null mice, while the expression of TLR-4 in TLR-4 null mice in the model group was significantly higher than that in sham group, with the statistical difference (P < 0.05). The expression of inflammatory factors in TLR-4 null mice and wild homozygous mice in the model group was significantly higher than that in sham group. The expression of all factors in group A with TLR-4 null was significantly lower than that in group B with wild homozygous type, with the statistical difference (P < 0.05).

Conclusions: TLR-4/NF-κB pathway is closely related to the myocardial ischemia reperfusion injury, which plays its role through the release of inflammatory cytokines.

Keywords: Myocardial ischemia reperfusion; NF-κB; Toll-like receptor 4.