Critical role of TLR-4/NF-κB pathway in upregulation mechanism of cerebral ischemia reperfusion injury of mouse

Abstract

The objective of this study is to investigate the expression of TLR-4/ NF-κB pathway in the cerebral ischemia injury of male adult mice. TLR-4 mutant (HeJ) mice and TLR-4 wild (HeN) mice were divided into the stroke model group and sham group. The stroke model was made by transient cerebral ischemia through middle cerebral artery occlusion (MCAO), while mice in the sham group were manipulated in the same way, but the MCA was not occluded. The brain 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 pro-inflammatory mediators. The expression of NF-κB in HeJ mice after the cerebral I/R was significantly lower than that in HeN mice. For the stroke model group and sham group, the expression of TLR-4 in HeN mice was all significantly higher than that in HeJ mice, while the expression of TLR-4 in HeJ mice in the stroke model group was significantly higher than that in sham group. The expression of all pro-inflammatory mediators with HeJ was significantly lower than that in HeN mice. Together, these data concluded that TLR-4/NF-κB pathway is closely related to the cerebral I/R injury, which plays its role through the release of pro-inflammatory cytokines..