Premium
Cerebralcare Granule®attenuates blood‐brain barrier disruption after middle cerebral artery occlusion in rats
Author(s) -
Han Jing-Yan,
Huang Ping,
Liu Yu-Ying,
Hu Bai-He,
Chang Xing,
Zhao Xin-Rong,
Li Quan,
Wei Xiao-Hong,
Wang Chuan-She,
Fan Jing-Yu,
Zhou Chang-Man
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb646
Subject(s) - occludin , blood–brain barrier , extravasation , tight junction , evans blue , medicine , ischemia , middle cerebral artery , pathology , western blot , chemistry , central nervous system , biochemistry , gene
Cerebralcare Granule®(CG) is a compound Chinese Medicine. In this study, we examined the effect of CG on the blood‐brain barrier (BBB) disruption in a focal cerebral ischemia/reperfusion rat model. Male Sprague‐Dawly rats (250 to 300 g) were subjected to 1h middle cerebral artery occlusion (MCAO). CG (0.4 g/kg and 0.8 g/kg) was administrated orally 3h after reperfusion for the first time and then once daily up to 6 days. The results showed that Evans blue extravasation, brain water content, albumin leakage, infarction volumes and neurological deficits were increased in MCAO rats, and were attenuated significantly by CG treatment. Magnetic Resonance Imaging and electron microscopy further confirmed the brain edema reduction in CG‐treated rats. Treatment with CG improved cerebral blood flow. Western blot analysis and confocal microscopy show that the tight junction proteins claudin‐5, Junctional adhesion molecule‐1, occludin and zonula occluden‐1 between endothelial cells were significantly degradated, but the protein expression of caveolin‐1, the principal marker of caveolae in endothelial cells, increased after ischemia, all of which were alleviated by CG. In conclusion, post‐treatment with CG significantly reduced BBB permeability and brain edema, which were correlated with preventing the tight junction proteins degradation and inhibiting caveolin‐1 expression in the endothelial cells.