Baicalin Attenuates Focal Cerebral Ischemic Reperfusion Injury by Inhibition of Protease-Activated Receptor-1 and Apoptosis

Objective: To investigate the neuro-protective effects of baicaiin in Wistar rats with focal cerebral ischemic reperfusion injury. Methods: Ninety adult male Wistar rats weighing 320-350 g were randomly divided into the following groups (n=5): (a) sham control group; (b) vehicle group, subjected to...

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Veröffentlicht in:Chinese journal of integrative medicine 2014-02, Vol.20 (2), p.116-122
1. Verfasser: 周庆博 段成竹 贾青 刘萍 李鲁杨
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Sprache:eng
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Zusammenfassung:Objective: To investigate the neuro-protective effects of baicaiin in Wistar rats with focal cerebral ischemic reperfusion injury. Methods: Ninety adult male Wistar rats weighing 320-350 g were randomly divided into the following groups (n=5): (a) sham control group; (b) vehicle group, subjected to middle cerebral artery occlusion and received vehicle intraperitoneally; (c-e) baicalin groups, which were subjected to the middle cerebral artery occlusion and treated with baicalin 25, 50 and 100 mg/kg, respectively. The neurological scores were determined at postoperative 1, 3 and 7 d after the treatment. The expression of protease-activated receptor-1 (PAR-1), PAR-1 mRNA and Caspase-3 were determined using Western blot, reverse transcription polymerase chain reaction (RT- PCR) analysis and immunohistochemistry, respectively. Results: Significant decrease was noted in the neurological score in the baicalin group compared with that of the vehicle group (P〈0.01). Additionally, down-regulation of PAR-1 mRNA, PAR-1 and Caspase-3 was observed in the baicalin groups compared with those obtained from the vehicle group (P〈0.01). Compared with the low-dose baicalin group (25 mg/kg), remarkable decrease was noted in neurological score, and the expression of PAR-1 mRNA, PAR-1 as well as Caspase-3 in the high-dose group (P〈0.05). Conclusion: Baicalin showed neuro-protective effects in focal cerebral ischemic reperfusion injury through inhibiting the expression of PAR-1 and apoptosis.
ISSN:1672-0415
1993-0402
DOI:10.1007/s11655-013-1441-7