Neuroprotective effect of paeoniflorin on cerebral ischemic rat by activating adenosine A 1 receptor in a manner different from its classical agonists

Da Liu, Ke Qiang Xie, Xin Quan Ji, Yang Ye, Cheng Liang Jiang, Xing Zu Zhu

Research output: Contribution to journalArticle

103 Citations (Scopus)

Abstract

1. The effects of paeoniflorin (PF), a compound isolated from Paeony radix, on neurological impairment and histologically measured infarction volume following transient and permanent focal ischemia were examined in Sprague-Dawley rats. 2. In transient ischemia model, rats were subjected to a 1.5-h occlusion of the middle cerebral artery (MCA). The administration of PF (2.5 and 5mg kg -1, s.c.) produced a dose-dependent decrease in both neurological impairment and the histologically measured infarction volume. Similar results were also obtained when PF (2.5, 5, and 10mg kg -1, s.c.) was given in permanent ischemia model. 3. The neuroprotective effect of PF (10mg kg -1, s.c.) was abolished by pretreatment of DPCPX (0.25mg kg -1, s.c.), a selective adenosine A 1 receptor (A 1R) antagonist. 4. PF (10, 40, and 160mg kg -1, i.v.) had no effect on mean arterial pressure (MAP) and heart rates (HR) in the conscious rat. Additionally, PF (10 -3 mol l -1) had no effect on noradrenaline- (NA-) or high K + concentration-induced contractions of isolated rabbit primary artery. 5. In competitive binding experiments, PF did not compete with the binding of [ 3H]DPCPX, but displaced the binding of [ 3H]NECA to the membrane preparation of rat cerebral cortex. This binding manner was distinguished from the classical A 1R agonists. 6. The results demonstrated that activation of A 1R might be involved in PF-induced neuroprotection in cerebral ischemia in rat. However, PF had no 'well-known' cardiovascular side effects of classical A 1R agonists. The results suggest that PF might have the potential therapeutic value as an anti-stroke drug.

Original languageEnglish (US)
Pages (from-to)604-611
Number of pages8
JournalBritish Journal of Pharmacology
Volume146
Issue number4
DOIs
StatePublished - Oct 1 2005
Externally publishedYes

Fingerprint

Neuroprotective Agents
Adenosine
Ischemia
Infarction
peoniflorin
Adenosine-5'-(N-ethylcarboxamide)
Paeonia
Competitive Binding
Middle Cerebral Artery Infarction
Brain Ischemia
Cerebral Cortex
Sprague Dawley Rats
Norepinephrine
Arterial Pressure
Arteries
Heart Rate
Stroke
Rabbits
Membranes

Keywords

  • Adenosine A receptor
  • Cardiovascular side effect
  • Neuroprotective effect
  • Paeoniflorin
  • Permanent cerebral ischemia
  • Transient cerebral ischemia

ASJC Scopus subject areas

  • Pharmacology

Cite this

Neuroprotective effect of paeoniflorin on cerebral ischemic rat by activating adenosine A 1 receptor in a manner different from its classical agonists. / Liu, Da; Xie, Ke Qiang; Ji, Xin Quan; Ye, Yang; Jiang, Cheng Liang; Zhu, Xing Zu.

In: British Journal of Pharmacology, Vol. 146, No. 4, 01.10.2005, p. 604-611.

Research output: Contribution to journalArticle

Liu, Da ; Xie, Ke Qiang ; Ji, Xin Quan ; Ye, Yang ; Jiang, Cheng Liang ; Zhu, Xing Zu. / Neuroprotective effect of paeoniflorin on cerebral ischemic rat by activating adenosine A 1 receptor in a manner different from its classical agonists. In: British Journal of Pharmacology. 2005 ; Vol. 146, No. 4. pp. 604-611.
@article{62f72f876a0d48dc852463643c940abd,
title = "Neuroprotective effect of paeoniflorin on cerebral ischemic rat by activating adenosine A 1 receptor in a manner different from its classical agonists",
abstract = "1. The effects of paeoniflorin (PF), a compound isolated from Paeony radix, on neurological impairment and histologically measured infarction volume following transient and permanent focal ischemia were examined in Sprague-Dawley rats. 2. In transient ischemia model, rats were subjected to a 1.5-h occlusion of the middle cerebral artery (MCA). The administration of PF (2.5 and 5mg kg -1, s.c.) produced a dose-dependent decrease in both neurological impairment and the histologically measured infarction volume. Similar results were also obtained when PF (2.5, 5, and 10mg kg -1, s.c.) was given in permanent ischemia model. 3. The neuroprotective effect of PF (10mg kg -1, s.c.) was abolished by pretreatment of DPCPX (0.25mg kg -1, s.c.), a selective adenosine A 1 receptor (A 1R) antagonist. 4. PF (10, 40, and 160mg kg -1, i.v.) had no effect on mean arterial pressure (MAP) and heart rates (HR) in the conscious rat. Additionally, PF (10 -3 mol l -1) had no effect on noradrenaline- (NA-) or high K + concentration-induced contractions of isolated rabbit primary artery. 5. In competitive binding experiments, PF did not compete with the binding of [ 3H]DPCPX, but displaced the binding of [ 3H]NECA to the membrane preparation of rat cerebral cortex. This binding manner was distinguished from the classical A 1R agonists. 6. The results demonstrated that activation of A 1R might be involved in PF-induced neuroprotection in cerebral ischemia in rat. However, PF had no 'well-known' cardiovascular side effects of classical A 1R agonists. The results suggest that PF might have the potential therapeutic value as an anti-stroke drug.",
keywords = "Adenosine A receptor, Cardiovascular side effect, Neuroprotective effect, Paeoniflorin, Permanent cerebral ischemia, Transient cerebral ischemia",
author = "Da Liu and Xie, {Ke Qiang} and Ji, {Xin Quan} and Yang Ye and Jiang, {Cheng Liang} and Zhu, {Xing Zu}",
year = "2005",
month = "10",
day = "1",
doi = "10.1038/sj.bjp.0706335",
language = "English (US)",
volume = "146",
pages = "604--611",
journal = "British Journal of Pharmacology",
issn = "0007-1188",
publisher = "Wiley-Blackwell",
number = "4",

}

TY - JOUR

T1 - Neuroprotective effect of paeoniflorin on cerebral ischemic rat by activating adenosine A 1 receptor in a manner different from its classical agonists

AU - Liu, Da

AU - Xie, Ke Qiang

AU - Ji, Xin Quan

AU - Ye, Yang

AU - Jiang, Cheng Liang

AU - Zhu, Xing Zu

PY - 2005/10/1

Y1 - 2005/10/1

N2 - 1. The effects of paeoniflorin (PF), a compound isolated from Paeony radix, on neurological impairment and histologically measured infarction volume following transient and permanent focal ischemia were examined in Sprague-Dawley rats. 2. In transient ischemia model, rats were subjected to a 1.5-h occlusion of the middle cerebral artery (MCA). The administration of PF (2.5 and 5mg kg -1, s.c.) produced a dose-dependent decrease in both neurological impairment and the histologically measured infarction volume. Similar results were also obtained when PF (2.5, 5, and 10mg kg -1, s.c.) was given in permanent ischemia model. 3. The neuroprotective effect of PF (10mg kg -1, s.c.) was abolished by pretreatment of DPCPX (0.25mg kg -1, s.c.), a selective adenosine A 1 receptor (A 1R) antagonist. 4. PF (10, 40, and 160mg kg -1, i.v.) had no effect on mean arterial pressure (MAP) and heart rates (HR) in the conscious rat. Additionally, PF (10 -3 mol l -1) had no effect on noradrenaline- (NA-) or high K + concentration-induced contractions of isolated rabbit primary artery. 5. In competitive binding experiments, PF did not compete with the binding of [ 3H]DPCPX, but displaced the binding of [ 3H]NECA to the membrane preparation of rat cerebral cortex. This binding manner was distinguished from the classical A 1R agonists. 6. The results demonstrated that activation of A 1R might be involved in PF-induced neuroprotection in cerebral ischemia in rat. However, PF had no 'well-known' cardiovascular side effects of classical A 1R agonists. The results suggest that PF might have the potential therapeutic value as an anti-stroke drug.

AB - 1. The effects of paeoniflorin (PF), a compound isolated from Paeony radix, on neurological impairment and histologically measured infarction volume following transient and permanent focal ischemia were examined in Sprague-Dawley rats. 2. In transient ischemia model, rats were subjected to a 1.5-h occlusion of the middle cerebral artery (MCA). The administration of PF (2.5 and 5mg kg -1, s.c.) produced a dose-dependent decrease in both neurological impairment and the histologically measured infarction volume. Similar results were also obtained when PF (2.5, 5, and 10mg kg -1, s.c.) was given in permanent ischemia model. 3. The neuroprotective effect of PF (10mg kg -1, s.c.) was abolished by pretreatment of DPCPX (0.25mg kg -1, s.c.), a selective adenosine A 1 receptor (A 1R) antagonist. 4. PF (10, 40, and 160mg kg -1, i.v.) had no effect on mean arterial pressure (MAP) and heart rates (HR) in the conscious rat. Additionally, PF (10 -3 mol l -1) had no effect on noradrenaline- (NA-) or high K + concentration-induced contractions of isolated rabbit primary artery. 5. In competitive binding experiments, PF did not compete with the binding of [ 3H]DPCPX, but displaced the binding of [ 3H]NECA to the membrane preparation of rat cerebral cortex. This binding manner was distinguished from the classical A 1R agonists. 6. The results demonstrated that activation of A 1R might be involved in PF-induced neuroprotection in cerebral ischemia in rat. However, PF had no 'well-known' cardiovascular side effects of classical A 1R agonists. The results suggest that PF might have the potential therapeutic value as an anti-stroke drug.

KW - Adenosine A receptor

KW - Cardiovascular side effect

KW - Neuroprotective effect

KW - Paeoniflorin

KW - Permanent cerebral ischemia

KW - Transient cerebral ischemia

UR - http://www.scopus.com/inward/record.url?scp=27144558321&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=27144558321&partnerID=8YFLogxK

U2 - 10.1038/sj.bjp.0706335

DO - 10.1038/sj.bjp.0706335

M3 - Article

C2 - 16086036

AN - SCOPUS:27144558321

VL - 146

SP - 604

EP - 611

JO - British Journal of Pharmacology

JF - British Journal of Pharmacology

SN - 0007-1188

IS - 4

ER -