BACKGROUND: Nitric oxide (NO) and related pathways are thought to play an important role in the pathogenesis of Parkinson's disease (PD). Our in vitro experiments suggested that green tea polyphenols (GTP) might protect dopamine neurons through inhibition of NO and reactive oxygen species (ROS). METHODS: Immunohistochemistry, terminal deoxynucleotidyl transferase-mediated dUTP Nick End Labeling assay, electron spin resonance spin trapping, enzyme linked immunosorbent assay, and molecular biological methods were used to investigate the effects of GTP in an unilateral 6-hydroxydopamine (6-OHDA)-treated rat model of PD. RESULTS: GTP treatment dose-dependently protected dopaminergic neurons by preventing from midbrain and striatal 6-OHDA-induced increase in 1) both ROS and NO levels, 2) lipid peroxidation, 3) nitrite/nitrate content, 4) inducible nitric oxide synthase, and 5) protein-bound 3-nitro-tyrosine. Moreover, GTP treatment dose-dependently preserved the free radical scavenging capability of both the midbrain and the striatum. CONCLUSIONS: These results support the in vivo protection of GTP against 6-OHDA and suggest that GTP treatment might represent a neuroprotective treatment of PD.
BACKGROUND:Nitric oxide (NO) and related pathways are thought to play an important role in the pathogenesis of Parkinson's disease (PD). Our in vitro experiments suggested that green tea polyphenols (GTP) might protect dopamine neurons through inhibition of NO and reactive oxygen species (ROS). METHODS: Immunohistochemistry, terminal deoxynucleotidyl transferase-mediated dUTP Nick End Labeling assay, electron spin resonance spin trapping, enzyme linked immunosorbent assay, and molecular biological methods were used to investigate the effects of GTP in an unilateral 6-hydroxydopamine (6-OHDA)-treated rat model of PD. RESULTS:GTP treatment dose-dependently protected dopaminergic neurons by preventing from midbrain and striatal 6-OHDA-induced increase in 1) both ROS and NO levels, 2) lipid peroxidation, 3) nitrite/nitrate content, 4) inducible nitric oxide synthase, and 5) protein-bound 3-nitro-tyrosine. Moreover, GTP treatment dose-dependently preserved the free radical scavenging capability of both the midbrain and the striatum. CONCLUSIONS: These results support the in vivo protection of GTP against 6-OHDA and suggest that GTP treatment might represent a neuroprotective treatment of PD.
Authors: Katherine E Strathearn; Gad G Yousef; Mary H Grace; Susan L Roy; Mitali A Tambe; Mario G Ferruzzi; Qing-Li Wu; James E Simon; Mary Ann Lila; Jean-Christophe Rochet Journal: Brain Res Date: 2014-02-03 Impact factor: 3.252
Authors: Aurélie de Rus Jacquet; Michael Timmers; Sin Ying Ma; Andrew Thieme; George P McCabe; Jay Hansford C Vest; Mary Ann Lila; Jean-Christophe Rochet Journal: J Ethnopharmacol Date: 2017-02-15 Impact factor: 4.360