Neurochemical Research

, Volume 35, Issue 8, pp 1147–1155

Spatio-Temporal Distribution of Inflammatory Reaction and Expression of TLR2/4 Signaling Pathway in Rat Brain Following Permanent Focal Cerebral Ischemia

Authors

  • Xian-kun Tu
    • Department of NeurosurgeryThe Affiliated Union Hospital of Fujian Medical University
    • Department of NeurosurgeryThe Affiliated Union Hospital of Fujian Medical University
  • Song-sheng Shi
    • Department of NeurosurgeryThe Affiliated Union Hospital of Fujian Medical University
  • Chun-hua Wang
    • Department of NeurosurgeryThe Affiliated Union Hospital of Fujian Medical University
  • Guo-liang Zhang
    • Department of NeurosurgeryThe Affiliated Union Hospital of Fujian Medical University
  • Tian-rui Ni
    • Department of NeurosurgeryThe Affiliated Union Hospital of Fujian Medical University
  • Chun-mei Chen
    • Department of NeurosurgeryThe Affiliated Union Hospital of Fujian Medical University
  • Rui Wang
    • Department of NeurosurgeryThe Affiliated Union Hospital of Fujian Medical University
  • Jian-wen Jia
    • Department of NeurosurgeryThe Affiliated Union Hospital of Fujian Medical University
  • Qi-min Song
    • Department of NeurosurgeryThe Affiliated Union Hospital of Fujian Medical University
Original Paper

DOI: 10.1007/s11064-010-0167-6

Cite this article as:
Tu, X., Yang, W., Shi, S. et al. Neurochem Res (2010) 35: 1147. doi:10.1007/s11064-010-0167-6

Abstract

Toll-like receptors (TLRs) are considered to mediate the inflammatory reaction, which are involved in the pathophysiological processes of cerebral ischemia injury. To elucidate the possible role of inflammatory reaction and TLR2/4 signaling pathway in cerebral ischemia, in the present study, we explored the spatio-temporal distribution of inflammatory reaction, and further investigated the time-course expression of TLR2/4 and the downstream effector molecules after focal cerebral ischemia in rats. Sprague–Dawley rats underwent permanent middle cerebral artery occlusion (pMCAO) for 6, 12, 24, 48 and 72 h. Neurological deficit, cerebral infarction and neutrophil infiltration were measured at different time points following pMCAO. Expression of TLR2/4 were examined by immunohistochemistry, reverse transcription-polymerase chain reaction (RT-PCR) and western blot. Nuclear factor-kappaB (NF-κB) and cyclooxygenase-2 (COX-2) were determined by western blot. Serum content of tumor necrosis factor-α (TNF-α) was detected by enzyme-linked immunosorbent assay (ELISA). Experimental results showed that pMCAO caused an increase of neutrophil infiltration in infarcted brain tissue, with a peaked activity at 24 h of ischemia. The inflammatory molecules including TLR2, TLR4, NF-κB, COX-2 and TNF-α were significantly increased after pMCAO, especially during 12–24 h of ischemia, which were correlated with pMCAO-induced brain injury and cerebral inflammation. Our studies suggested that TLR2/4 signaling pathway likely aggravated ischemic brain injury through mediating the inflammatory reaction. TLR2/4 signaling pathway may be a promising therapeutic target for cerebral ischemia injury.

Keywords

Cerebral ischemiaCyclooxygenase-2InflammationNuclear factor-kappaBToll-like receptorsTumor necrosis factor-αStroke

Copyright information

© Springer Science+Business Media, LLC 2010