연구자료

INTRODUCTION Panax ginseng Meyer is a perennial herb of the family Araliaceae. For millennia, P. ginseng has been traditionally used as a medicine in Asia, particularly in Korea, China and Japan. More recently, ginseng has become popular globally [1]. Its roots have been traditionally used to revitalize the body and mind, increase physical strength, prevent aging and increase vigor [2]. The main active pharmacological compounds in P. ginseng are ginsenosides, which are derivatives of triterpenoid dammarane. More than 31 ginsenosides has been isolated from natural and processed P. ginseng, and novel ginsenosides continue to be reported [3,4]. All ginsenosides have a common four-ring hydrophobic, steroid-like structure with attached sugar moieties. The specific action of each ginsenoside might depend on the diversity of the sugar components, and the number and position of the sugar moieties [5]. Each ginsenoside has different pharmacological effects, and a single ginsenoside can produce multiple effects in the same tissue [6,7]. Asian and Western scientists have introduced a new pharmacological concept of P. ginseng, with a wide range of actions on different body systems. Recently, ginsenosides have been shown to produce a number of beneficial effects in the nervous system [8-10]. NEUROPROTECTIVE EFFECTS OF PANAX GINSENG Neuroprotection can be defined as a therapeutic intervention that prevents the death of vulnerable neurons, slows disease progression, and delays transition from the preclinical to the clinical stage [11]. Neuroprotection also refers to the inhibition or delay of neuronal death by virtue of the slowing or blocking of neuroprodegenerative processes either prematurely or in old age [12,13]. The possible influence of P. ginseng in neuroprotection is becoming increasingly recognized and researched. Parkinson’s disease Parkinson’s disease (PD) is a progressive neurodegenerative disease that afflicts an estimated 2% of the global population over the age of 60 years. The mechanisms leading to PD rely on interactions between environmental and genetic factors, and are characterized by the accumulation and aggregation of misfolded α-synuclein. Neuropathological hallmarks are profound loss of dopaminergic neurons in the substantia nigra (SN) of the midbrain and accumulation of α-synuclein aggregates into Lewy bodies and Lewy neuritis [13]. The main symptoms of PD are motor disorders including tremor, rigidity, bradykinesia and postural instability, and non-motorrelated disorders including sleep disturbance, autonomic dysfunction, cognitive deficits, depression, and olfactory deficits. These symptoms result from the progressive degeneration of the nigrostriatal dopaminergic pathway. To date, most PD therapies provide only symptomatic treatment, and no drug has been found that prevents the progressive loss of dopaminergic neurons in PD patients [14,15].