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Title: Reduced cerebral ischemia-reperfusion injury in Toll-like receptor 4 deficient mice

Journal Article · · Biochemical and Biophysical Research Communications
OSTI ID:20979792
 [1];  [1];  [2];  [1];  [1];  [1]
  1. Department of Neurology, DaPing Hospital, Third Military Medical University, ChangJiang Branch Road 10, DaPing, YuZhong District, Chongqing 400042 (China)
  2. State Key Laboratory of Trauma, Burn, and Combined Wound, Institute of Surgery and Daping Hospital, Third Military Medical University, Chongqing 400042 (China)

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.

OSTI ID:
20979792
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 353, Issue 2; Other Information: DOI: 10.1016/j.bbrc.2006.12.057; PII: S0006-291X(06)02711-2; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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