Literature DB >> 23504578

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

Qing-bo Zhou1, Cheng-zhu Duan, Qing Jia, Ping Liu, Lu-yang Li.   

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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Year:  2013        PMID: 23504578     DOI: 10.1007/s11655-013-1441-7

Source DB:  PubMed          Journal:  Chin J Integr Med        ISSN: 1672-0415            Impact factor:   1.978


  26 in total

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4.  Hemostatic activation in acute ischemic stroke.

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5.  The contribution of protease-activated receptor 1 to neuronal damage caused by transient focal cerebral ischemia.

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3.  Protective Effects of Baicalin on Aβ₁₋₄₂-Induced Learning and Memory Deficit, Oxidative Stress, and Apoptosis in Rat.

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5.  Baicalin ameliorates isoproterenol-induced acute myocardial infarction through iNOS, inflammation, oxidative stress and P38MAPK pathway in rat.

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6.  Baicalin protects against thrombin induced cell injury in SH-SY5Y cells.

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