Effects of pretreatment with methanol extract of Peucedani Radix on transient ischemic brain injury in mice
Stroke is the second most common cause of death and may result in various disabilities; thus, identification of neuroprotective therapeutic agents is important. Peucedani Radix (PR), the root of , is a well-known remedy for damp and phlegm in Korean medicine and has also been shown to exert antioxid...
Gespeichert in:
Veröffentlicht in: | Chinese medicine 2017-10, Vol.12 (1), p.30-30, Article 30 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Stroke is the second most common cause of death and may result in various disabilities; thus, identification of neuroprotective therapeutic agents is important. Peucedani Radix (PR), the root of
, is a well-known remedy for damp and phlegm in Korean medicine and has also been shown to exert antioxidant and anti-inflammatory activities. This study was performed to investigate the mechanism underlying the anti-inflammatory effect of methanol extract of PR (PRex) on cerebral ischemic injury.
C57BL/6 male mice were orally administered PRex (20, 60, or 200 mg/kg) at 2 days, 1 day, and 1 h prior to middle cerebral artery occlusion (MCAO). Twenty-four hours after MCAO, the infarct volume was measured and the neurological deficit score was assessed. The inflammatory-related substances in the ipsilateral hemisphere were determined by western blotting, DCFH-DA assay, TBARS assay, and ELISA.
PRex pretreatment significantly decreased the infarct volume at 24 h after MCAO. Moreover, PRex effectively suppressed the expression of iNOS, ROS, MDA, and pro-inflammatory cytokines, such as IL-1β and TNF-α, in brain tissue of mice with MCAO-induced brain injury.
PRex protected neurons from ischemic brain injury in mice through its antioxidant and anti-inflammatory activities. Our results suggested that PR could be a promising candidate in the therapy of ischemia-induced brain damage. |
---|---|
ISSN: | 1749-8546 1749-8546 |
DOI: | 10.1186/s13020-017-0151-z |