期刊
INFLAMMATION
卷 34, 期 5, 页码 463-470出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-010-9254-8
关键词
baicalin; cerebral ischemia; cyclooxygenase-2; inducible nitric oxide synthase; inflammation; interleukin-1 beta; nuclear factor-kappa B; toll-like receptors; tumor necrosis factor-alpha
资金
- Affiliated Union Hospital of Fujian Medical University
- Fujian Medical University [JS0610]
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-kappa B) 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-kappa B, 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-alpha) and interleukin-1 beta (IL-1 beta) were detected by ELISA. Baicalin reduced cerebral infarct area and infarct volume. Baicalin reduced the expression of TLR2/4 and NF-kappa B, decreased the expression and activity of iNOS and COX-2 in rat brain. Baicalin also attenuated the serum content of TNF-alpha and IL-1 beta. Our results suggest that baicalin inhibits the TLR2/4 signaling pathway in cerebral ischemia, which may be a mechanism underlying the baicalin's neuroprotection.
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