Protective Effects of Red Ginseng Oil against Aβ25-35-Induced Neuronal Apoptosis and Inflammation in PC12 Cells

One of pathological characteristics of Alzheimer's disease (AD), aggregation and deposition of beta amyloid (A beta), has been accepted as a potent activator of neuronal cell death. Red ginseng is well-known for various pharmacological activities, but most studies have been focused on red ginseng water extract (RGW), which has resulted in the conception of the present study of red ginseng oil (RGO) against A beta(25-35)-induced neurotoxicity. Cytotoxicity and apoptosis induction by A beta were verified and the underlying mechanism by which RGO inhibited neuronal cell death, mitochondria dysfunction and NF-kappa B pathway related protein markers were evaluated. RGO attenuated A beta(25-35)-induced apoptosis, not only by inhibiting calcium influx, but also by reducing mitochondrial membrane potential loss. RGO significantly decreased Bax, whereas increased Bcl-2 and inactivated of caspase-3 and -9 and PARP-1 stimulated by A beta(25-35). Anti-neuroinflammatory effect of RGO was demonstrated by downregulating c-Jun N-terminal kinase (JNK) and p38, resulting in inhibiting of the NF-kappa B pathway and thereby suppressing the expressions of pro-inflammatory mediators such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), prostaglandin E-2 (PGE(2)), nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha). The present study revealed that RGO is a potential natural resource of the functional foods industry as well as a promising candidate of multi-target neuronal protective agent for the prevention of AD.