Department of Neurology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
J Ethnopharmacol. 2011 Oct 31;138(1):135-41. doi: 10.1016/j.jep.2011.08.068. Epub 2011 Sep 8.
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.
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.
Pretreatment with ginsenoside Rd in SD rats (10mg/kg for 7 days) or in cultured cortical neurons (2.5 or 5μmol/L for 12h) reduced OA-induced neurotoxicity and tau hyperphosphorylation by enhancing the activities of PP-2A.
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.
人参,一种传统的中药,在亚洲已经被广泛用于恢复疾病和增强健康的身体,大约有 5000 年的历史。本研究旨在探讨人参皂甙 Rd 对 OA 诱导的毒性的可能神经保护作用。
人参皂甙 Rd 用于阿尔茨海默病(AD)的 tauopathy 模型。为了模拟体内或体外 tau 过度磷酸化,蛋白磷酸酶抑制剂 okadaic acid(OA)被双侧微注入成年雄性 Sprague-Dawley(SD)大鼠的脑室,或添加到培养的皮质神经元的培养基中。测量 tau 的磷酸化水平和蛋白磷酸酶 2A(PP-2A)的活性,并与人参皂甙 Rd 预处理组进行比较。
人参皂甙 Rd 在 SD 大鼠(10mg/kg,7 天)或培养的皮质神经元(2.5 或 5μmol/L,12 小时)中的预处理通过增强 PP-2A 的活性,减少了 OA 诱导的神经毒性和 tau 过度磷酸化。
本工作的结果表明,人参皂甙 Rd 对 SD 大鼠和培养的皮质神经元具有保护作用,防止 OA 诱导的毒性。可能的神经保护机制可能是人参皂甙 Rd 通过增加 PP-2A 的活性来减少 OA 诱导的 tau 过度磷酸化。因此,这项研究预示着人参皂甙 Rd 可能是 AD 和其他 tau 病理学相关神经元退行性疾病的潜在预防药物候选物。