Protective effect of baicalin on inflammatory injury following transient focal cerebral ischemia-reperfusion in rats
- VernacularTitle:黄芩苷对大鼠局灶性短暂性脑缺血再灌继发炎性损伤的保护作用
- Author:
Changhan OUYANG
;
Jiliang WU
- Publication Type:Journal Article
- Keywords:
baicalin;
cerebral ischemia;
intracellular adhesion molecule-1;
nitric oxide synthase;
NF-kappa B;
interleukin-1
- From:
Chinese Journal of Pharmacology and Toxicology
2006;20(4):288-294
- CountryChina
- Language:Chinese
-
Abstract:
AIM To investigate if the protective effect of baicalin on cerebral injury induced by transient focal ischemia is related to modulation of expressions of inflammatory cytokines or adhesive molecules. METHODS Transient focal cerebral ischemia injury model in rats was induced by occlusion of the right middle cerebral artery for 2 h, followed by 24 h reperfusion. The infarct volume and neurological deficit were determined by TTC staining and the scoring method of Longa et al. The expression of intracellular adhesion molecule-1 (ICAM-1), neutrophils infiltration, and myeloperoxidase (MPO) activity in brain were measured by immunohistochemistry, hematoxylin-eosin staining, and spectrophotometer, respectively. Semiquantitative RT-PCR was employed to assess the expression of inducible nitric oxide synthase (iNOS) mRNA. The level of interleukin-1 (IL-1) in brain was assayed by radioimmunoassay. The expression of nuclear factor-κB (NF-κB) protein was evaluated by Western blot. RESULTS After transient cerebral ischemia, MPO activity and the expression of ICAM-1 in the periphery of ischemic cortex were significantly increased. Increase in iNOS mRNA and NF-κB protein expression was also shown in the ischemic area. Treatment with baicalin markedly reduced brain infarct volume and neurological deficit induced by ischemic insult, inhibited MPO activity, inflammatory cell infiltration, as well as expression of ICAM-1, iNOS and NF-κB, and decreased IL-1 level. CONCLUSION Baicalin may play a protective effect on cerebral ischemic injury through inhibiting the expression and release of the inflammatory mediators after cerebral ischemia.
