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Neuroprotective effect of the antiparkinsonian drug pramipexole against nigrostriatal dopaminergic degeneration in rotenone-treated mice.
Neurochem Int. 2009 Dec; 55(8):760-7.NI

Abstract

Pramipexole, an agonist for dopamine (DA) D2/D3-receptors, has been used to treat both early and advanced Parkinson's disease (PD). In this study, we examined the effect of pramipexole on DA neurons in a PD model of C57BL/6 mice, which were treated with rotenone (30 mg/kg, p.o.) daily for 28 days. Pramipexole (1 mg/kg, i.p.) was injected daily 30 min before each oral administration of rotenone. Chronic oral administration of rotenone caused a loss of DA neurons in the substantia nigra pars compacta (SNpc), motor deficits and the up-regulation of alpha-synuclein immunoreactivity in some surviving DA neurons. Pramipexole inhibited rotenone-induced DA neuronal death and motor deficits, and reduced immunoreactivity for alpha-synuclein. In addition, pramipexole inhibited the in vitro oligomerization of human wild-type alpha-synuclein by H(2)O(2)plus cytochrome c. To examine the neuroprotective effect of pramipexole against oxidative stress, we used a DJ-1-knockdown SH-SY5Y cell line and electron spin resonance (ESR) spectrometry. Simultaneous treatment with H(2)O(2) and pramipexole resulted in the significant protection of DJ-1-knockdown cells against cell death in a concentration-dependent manner. A high concentration of pramipexole directly scavenged hydroxyl radical (*OH) generated from H(2)O(2) and Fe(2+). Furthermore, pramipexole increased Bcl-2 immunoreactivity in DA neurons in the SNpc. These results suggest that pramipexole may protect DA neurons against exposure to rotenone by chronic oral administration, and this effect is mediated by multiple functions including scavenging of *OH and induction of Bcl-2 protein.

Authors+Show Affiliations

Department of Neurobiology, Kyoto Pharmaceutical University, Kyoto 607-8414, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19647776

Citation

Inden, Masatoshi, et al. "Neuroprotective Effect of the Antiparkinsonian Drug Pramipexole Against Nigrostriatal Dopaminergic Degeneration in Rotenone-treated Mice." Neurochemistry International, vol. 55, no. 8, 2009, pp. 760-7.
Inden M, Kitamura Y, Tamaki A, et al. Neuroprotective effect of the antiparkinsonian drug pramipexole against nigrostriatal dopaminergic degeneration in rotenone-treated mice. Neurochem Int. 2009;55(8):760-7.
Inden, M., Kitamura, Y., Tamaki, A., Yanagida, T., Shibaike, T., Yamamoto, A., Takata, K., Yasui, H., Taira, T., Ariga, H., & Taniguchi, T. (2009). Neuroprotective effect of the antiparkinsonian drug pramipexole against nigrostriatal dopaminergic degeneration in rotenone-treated mice. Neurochemistry International, 55(8), 760-7. https://doi.org/10.1016/j.neuint.2009.07.009
Inden M, et al. Neuroprotective Effect of the Antiparkinsonian Drug Pramipexole Against Nigrostriatal Dopaminergic Degeneration in Rotenone-treated Mice. Neurochem Int. 2009;55(8):760-7. PubMed PMID: 19647776.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotective effect of the antiparkinsonian drug pramipexole against nigrostriatal dopaminergic degeneration in rotenone-treated mice. AU - Inden,Masatoshi, AU - Kitamura,Yoshihisa, AU - Tamaki,Aya, AU - Yanagida,Takashi, AU - Shibaike,Tomonori, AU - Yamamoto,Atsuko, AU - Takata,Kazuyuki, AU - Yasui,Hiroyuki, AU - Taira,Takahiro, AU - Ariga,Hiroyoshi, AU - Taniguchi,Takashi, Y1 - 2009/08/06/ PY - 2009/04/17/received PY - 2009/07/23/revised PY - 2009/07/23/accepted PY - 2009/8/4/entrez PY - 2009/8/4/pubmed PY - 2010/1/26/medline SP - 760 EP - 7 JF - Neurochemistry international JO - Neurochem Int VL - 55 IS - 8 N2 - Pramipexole, an agonist for dopamine (DA) D2/D3-receptors, has been used to treat both early and advanced Parkinson's disease (PD). In this study, we examined the effect of pramipexole on DA neurons in a PD model of C57BL/6 mice, which were treated with rotenone (30 mg/kg, p.o.) daily for 28 days. Pramipexole (1 mg/kg, i.p.) was injected daily 30 min before each oral administration of rotenone. Chronic oral administration of rotenone caused a loss of DA neurons in the substantia nigra pars compacta (SNpc), motor deficits and the up-regulation of alpha-synuclein immunoreactivity in some surviving DA neurons. Pramipexole inhibited rotenone-induced DA neuronal death and motor deficits, and reduced immunoreactivity for alpha-synuclein. In addition, pramipexole inhibited the in vitro oligomerization of human wild-type alpha-synuclein by H(2)O(2)plus cytochrome c. To examine the neuroprotective effect of pramipexole against oxidative stress, we used a DJ-1-knockdown SH-SY5Y cell line and electron spin resonance (ESR) spectrometry. Simultaneous treatment with H(2)O(2) and pramipexole resulted in the significant protection of DJ-1-knockdown cells against cell death in a concentration-dependent manner. A high concentration of pramipexole directly scavenged hydroxyl radical (*OH) generated from H(2)O(2) and Fe(2+). Furthermore, pramipexole increased Bcl-2 immunoreactivity in DA neurons in the SNpc. These results suggest that pramipexole may protect DA neurons against exposure to rotenone by chronic oral administration, and this effect is mediated by multiple functions including scavenging of *OH and induction of Bcl-2 protein. SN - 1872-9754 UR - https://www.unboundmedicine.com/medline/citation/19647776/Neuroprotective_effect_of_the_antiparkinsonian_drug_pramipexole_against_nigrostriatal_dopaminergic_degeneration_in_rotenone_treated_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0197-0186(09)00230-7 DB - PRIME DP - Unbound Medicine ER -