Biol. Pharm. Bull. 28(1) 169—172 (2005)

genic medicine, and it has been used as a crude drug to treat stress-induced physiological changes, various allergic conditions, inflammation and cancer. An aqueous extract of the stem bark of A. senticosus HARMS (ASH) from Japan and its components, chlorogenic acid (CHA) and syringaresinol di-o-b-D-glucoside (SYG), markedly prevent the ulcerogenesis in rats subjected to restraint stress in water for 7 h. Among CHA, SYG, syringin and sesamin, components of the n-butanol extract prepared from ASH, sesamin suppressed the growth and induced apoptosis in KATO III cells. A study demonstrates that ASH has a specific actvity in the nigrostriatal dopaminerigic system and it results in protection against the development of parkinsonian bradykinesia and catalepsy reaction caused by 1-methyl-4-phenyl1,2,3,6-tetrahydropyridine (MPTP). However, it is unclear if the direct action of the ASH component, sesamin on the nigrostriatal DAergic system actually contributes to the prevention of Parkinson’s disease (PD) caused by exposure to rotenone. Selective nigral degeneration with inclusion formation with a-synuclein and ubiquitin was provoked by systemic administration of the herbicide rotenone through inhibition of mitochondrial complex I. The result raises the question of pesticide exposure and environmental neurotoxins in general, as a cause of PD. In such much dangerous information, it is equal to there being no means in which the agricultural chemical user protects the their own body as a category of the prevention medical treatment. The administration of exogenous glial cell line-derived neurotrophic factor (GDNF) or the delivery of GDNF via gene therapy can increase the apparent capacity of DA neurons to release their transmitter and protect and even rescue adult DA neuron from injury caused by 6-hydroxydopamine (6-OHDA) and MPTP. However, though this research is good news to the human who becomes PD, it is far from the feasibility still. In short, it is necessary to carry out the effort which does not become the PD even in now. In this study, we examined whether the ASH and sesamin have a preventive effect on bradykinesia, depressive behavior and the loss of tyrosine hydroxylase (TH) or GDNF-positive neurons in the midbrain of the rats using a PD model induced by rotenone. We herein report that ASH and sesamin act on the midbrain to suppress rotenone-induced depletion in DA cells and consequently prevents the parkinsonian bradykinesia and depressive behavior.