Reduced cerebral ischemia-reperfusion injury in Toll-like receptor 4 deficient mice.
Inflammatory reaction plays an important role in cerebral ischemia-reperfusion injury, however, its mechanism is still unclear. Our study aims to explore the function of Toll-like receptor 4 (TLR4) in the process of cerebral ischemia-reperfusion. We made middle cerebral artery ischemia-reperfusion model in mice with line embolism method. Compared with C3H/OuJ mice, scores of cerebral water content, cerebral infarct size and neurologic impairment in C3H/Hej mice were obviously lower after 6 h ischemia and 24 h reperfusion. Light microscopic and electron microscopic results showed that cerebral ischemia-reperfusion injury in C3H/Hej mice was less serious than that in C3H/OuJ mice. TNF-alpha and IL-6 contents in C3H/HeJ mice were obviously lower than that in C3H/OuJ mice with ELISA. The results showed that TLR4 participates in the process of cerebral ischemia-reperfusion injury probably through decrease of inflammatory cytokines. TLR4 may become a new target for prevention of cerebral ischemia-reperfusion injury. Our study suggests that TLR4 is one of the mechanisms of cerebral ischemia-reperfusion injury besides its important role in innate immunity.
Cao
Can-Xiang
CX
Department of Neurology, DaPing Hospital, The Third Military Medical University, ChangJiang Branch Road 10, DaPing, YuZhong District, Chongqing 400042, China.
Yang
Qing-Wu
QW
Lv
Feng-Lin
FL
Cui
Jie
J
Fu
Hua-Bin
HB
Wang
Jing-Zhou
JZ
D000818:Animals; D001921:Brain / Q000098:blood supply / Q000378:metabolism / Q000473:pathology; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology*; D002544:Cerebral Infarction / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D051379:Mice; D008809:Mice, Inbred C3H; D018345:Mice, Knockout; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology*; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism*
C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4