QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: jpet.106.104380v1 319/1/165    most recent Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Chen, D.-M. Articles by Zhu, X.-Z. Search for Related Content PubMed PubMed Citation Articles by Chen, D.-M. Articles by Zhu, X.-Z.

NEUROPHARMACOLOGY

Involvement of Multitargets in Paeoniflorin-Induced Preconditioning

Department of Pharmacology, Shanghai Institute of Materia Medica (D.-M.C., X.C., X.-Z.Z.) and The Research Centre for Proteome Analysis, Key Lab of Proteomics, Institute of Biochemistry and Cell Biology (R.Z.), Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China; and Department of Research and Development (L.X.), Jiangsu Hengrui Medicine Company, Shanghai, China

Paeoniflorin (PF) is the principal component of Paeoniae radix prescribed in traditional Chinese medicine. The delayed neuroprotection induced by PF preconditioning and its underlying mechanisms were investigated in rat middle cerebral artery occlusion (MCAO) and reperfusion model. At a dosage of 20 or 40 mg/kg, PF preconditioning 48 h before MCAO followed by 24-h reperfusion significantly reduced the mortality and infarct volume and reversed the neurological deficits caused by ischemia. Likewise, the ameliorative effects on mortality, infarct size, and neurological impairment induced by MCAO emerged as well when PF was administered 24 h, 48 h, or 5 days before MCAO at the dose of 20 mg/kg. Furthermore, comparative proteomics analysis was adopted to identify the differentially expressed proteins induced by PF preconditioning itself. The relative levels of 42 proteins were altered after PF preconditioning, among which 20 were elevated and 22 reduced. In summary, A₁ receptor-regulator of G protein signaling-K_ATP signaling, arachidonic acid cascade, nitric oxide system, markers of neuronal damage, mitochondrial damage-related molecules, and the mitogen-activated protein kinase and nuclear factor-B pathway are associated with the mechanisms of PF preconditioning.

Address correspondence to: Dr. Xing-Zu Zhu, Department of Pharmacology, Shanghai Institute of Materia Medica, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 555 Zu Chong Zhi Road, Zhangjiang Hi-Tech Park, Pudong Shanghai 201203, China. E-mail: xzzhu{at}mail.shcnc.ac.cn