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Baicalin attenuates focal cerebral ischemic reperfusion injury by inhibition of protease-activated receptor-1 and apoptosis

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Abstract

Objective

To investigate the neuro-protective effects of baicalin 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 (RTPCR) 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.

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Correspondence to Qing-bo Zhou  (周庆博).

Additional information

Supported by National Natural Science Foundation of China (No. 81072916), Shandong Science and Technique Foundation (No. 2005GG3202062), Shandong Traditional Chinese Medicine Administration Fund Program (No.2009-160) and Free Exploration Program of Shandong University (No.2009TS009)

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Zhou, Qb., Duan, Cz., Jia, Q. et al. Baicalin attenuates focal cerebral ischemic reperfusion injury by inhibition of protease-activated receptor-1 and apoptosis. Chin. J. Integr. Med. 20, 116–122 (2014). https://doi.org/10.1007/s11655-013-1441-7

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  • DOI: https://doi.org/10.1007/s11655-013-1441-7

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