Protective Effects of Green Tea Polyphenols Against Parkinson's Disease / 生物化学与生物物理进展

ABSTRACT

About 70% of Parkinson's pathogenesis comes from environment factor and one important of which is oxidative stress although the genetic factor plays an important role. The antioxidant of green tea polyphenols(GTP) and they can enter into plasma even penetrate blood brain barie provides an important condition for the protective effects of GTP against Parkinson's Disease(PD). In cellular model the protective mechanisms of GTP on PC12 and SH-SY5Y cells against apoptosis induced by 6-hydroxydopamine (6-OHDA) were investigated. GTP attenuated 6-OHDA-induced early apoptosis, prevented the decrease in mitochondrial membrane potential, suppressed accumulation of reactive oxygen species (ROS) and of intracellular free Ca2+. GTP also counteracted 6-OHDA-induced nitric oxide increase and over-expression of nNOS and iNOS, and decreased the level of protein bound 3-Nitro-tyrosine (3-NT). Using PD rat model injected by 6-OHDA, the effect of GTP were investigated on animal model. Results showed that GTP attenuated the injury in a dose and time dependent manner. Pretreatment of the animals with GTP decreased ROS and NO production, thiobarituric acid reactive substances content, nitrite/nitrate concentration, and protein bound 3-Nitro-tyrosine (3-NT) in brain homogenate of midbrain and striatum in a concentration and time dependent manner. NOS participated in the neuron death induced by 6-OHDA and it was found that the pretreatment with GTP could decrease the protein level of nNOS and iNOS. More neurons survived and less cells suffered apoptosis in the substantia nigra pars compacta (SNc) of GTP treated animal brain. These results suggest that oral administration of GTP increases the antioxidant level in the brain and protects the brain against cell death caused by 6-OHDA. The experimental results of present study support the neuroprotection of GTP and provided new strategy of preventing and curing Parkinson's diseases by ROS-NO pathway.