Inflammation

, Volume 34, Issue 5, pp 463–470

Baicalin Inhibits TLR2/4 Signaling Pathway in Rat Brain Following Permanent Cerebral Ischemia

  • Xian-kun Tu
  • Wei-zhong Yang
  • Song-sheng Shi
  • Ye Chen
  • Chun-hua Wang
  • Chun-mei Chen
  • Zhen Chen
Article

DOI: 10.1007/s10753-010-9254-8

Cite this article as:
Tu, X., Yang, W., Shi, S. et al. Inflammation (2011) 34: 463. doi:10.1007/s10753-010-9254-8

Abstract

Recent work from our laboratory demonstrated that baicalin attenuates inflammatory reaction and cerebral ischemia injury in rats. Toll-like receptor 2 and 4 (TLR2/4) and the downstream nuclear factor-kappa B (NF-κB) signaling pathway, which mediate the inflammatory reaction, are involved in the pathophysiological processes of cerebral ischemia. In this study, we investigated whether baicalin inhibits TLR2/4 signaling pathway in a rat model of permanent focal cerebral ischemia. Adult Sprague–Dawley rats underwent permanent middle cerebral artery occlusion (MCAO). Baicalin was administered by intraperitoneally injected twice at 2 and 12 h after the onset of ischemia. Cerebral infarct area and infarct volume were measured 24 h after MCAO. Expression of TLR2/4, NF-κB, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) were determined by RT-PCR or western blot. NO and PGE2 production in rat brain were measured 24 h after MCAO. Serum content of tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) were detected by ELISA. Baicalin reduced cerebral infarct area and infarct volume. Baicalin reduced the expression of TLR2/4 and NF-κB, decreased the expression and activity of iNOS and COX-2 in rat brain. Baicalin also attenuated the serum content of TNF-α and IL-1β. Our results suggest that baicalin inhibits the TLR2/4 signaling pathway in cerebral ischemia, which may be a mechanism underlying the baicalin’s neuroprotection.

KEY WORDS

baicalincerebral ischemiacyclooxygenase-2inducible nitric oxide synthaseinflammationinterleukin-1βnuclear factor-kappa Btoll-like receptorstumor necrosis factor-α

Copyright information

© Springer Science+Business Media, LLC 2010

Authors and Affiliations

  • Xian-kun Tu
    • 1
    • 2
  • Wei-zhong Yang
    • 1
    • 2
  • Song-sheng Shi
    • 1
  • Ye Chen
    • 3
  • Chun-hua Wang
    • 2
  • Chun-mei Chen
    • 1
  • Zhen Chen
    • 1
  1. 1.Department of NeurosurgeryThe Affiliated Union Hospital of Fujian Medical UniversityFuzhouChina
  2. 2.Fujian Neurosurgical Institute29# Xinquan Road, FuzhouFujianChina
  3. 3.Department of AnesthesiologyFujian Provincial HospitalFuzhouChina