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Paeoniflorin attenuates neuroinflammation and dopaminergic neurodegeneration in the MPTP model of Parkinson's disease by activation of adenosine A 1 receptor
Author(s) -
Liu HuaQing,
Zhang WeiYu,
Luo XueTing,
Ye Yang,
Zhu XingZu
Publication year - 2006
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0706732
Subject(s) - mptp , neuroprotection , dopaminergic , pharmacology , substantia nigra , neurodegeneration , neuroinflammation , tyrosine hydroxylase , parkinson's disease , paeoniflorin , medicine , chemistry , dopamine , endocrinology , inflammation , disease , high performance liquid chromatography , chromatography
1 This study examined whether Paeoniflorin (PF), the major active components of Chinese herb Paeoniae alba Radix, has neuroprotective effect in the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) mouse model of Parkinson's disease (PD). 2 Subcutaneous administration of PF (2.5 and 5 mg kg −1 ) for 11 days could protect tyrosine hydroxylase (TH)‐positive substantia nigra neurons and striatal nerve fibers from death and bradykinesia induced by four‐dose injection of MPTP (20 mg kg −1 ) on day 8. 3 When given at 1 h after the last dose of MPTP, and then administered once a day for the following 3 days, PF (2.5 and 5 mg kg −1 ) also significantly attenuated the dopaminergic neurodegeneration in a dose‐dependent manner. Post‐treatment with PF (5 mg kg −1 ) significantly attenuated MPTP‐induced proinflammatory gene upregulation and microglial and astrocytic activation. 4 Pretreatment with 0.3 mg kg −1 8‐cyclopentyl‐1,3‐dipropylxanthine, an adenosine A 1 receptor (A 1 AR) antagonist, 15 min before each dose of PF, reversed the neuroprotective and antineuroinflammatory effects of PF. 5 In conclusion, this study demonstrated that PF could reduce the MPTP‐induced toxicity by inhibition of neuroinflammation by activation of the A 1 AR, and suggested that PF might be a valuable neuroprotective agent for the treatment of PD.British Journal of Pharmacology (2006) 148 , 314–325. doi: 10.1038/sj.bjp.0706732