Protective effects of ginsenoside Rd against okadaic acid-induced neurotoxicity in vivo and in vitro.

Abstract Ethnopharmacological relevance Panax ginseng, a traditional Chinese herbal medicine, has been widely used to restore the disease and enhance the healthy body in Asia for about 5000 years. The present study aimed to investigate the possible neuroprotective effects of ginsenoside Rd against OA-induced toxicity. Materials and methods Ginsenoside Rd was used in tauopahy models of Alzheimer's disease (AD). To mimic the in vivo or in vitro tau hyperphosphorylation, okadaic acid (OA), a protein phosphatase inhibitor, was bilaterally micro-infused into the cerebral ventricle of adult male Sprague-Dawley (SD) rats, or added in media of cultured cortical neurons. The phosphorylation levels of tau and the activities of protein phosphatase 2A (PP-2A) were measured and compared with ginsenoside Rd pretreated groups. Results Pretreatment with ginsenoside Rd in SD rats (10 mg/kg for 7 days) or in cultured cortical neurons (2.5 or 5 μmol/L for 12 h) reduced OA-induced neurotoxicity and tau hyperphosphorylation by enhancing the activities of PP-2A. Conclusions The result of the present work implied that ginsenoside Rd protected SD rats and cultured cortical neurons against OA-induced toxicity. The possible neuroprotective mechanism may be that ginsenoside Rd decreases OA-induced the hyperphosphorylation of tau by the increase in activities of PP-2A. Thus, this study promises that ginsenoside Rd might be a potential preventive drug candidate for AD and other tau pathology-related neuronal degenerative diseases.