School of Chinese Medicine, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China.
Phytother Res. 2011 May;25(5):681-5. doi: 10.1002/ptr.3321. Epub 2010 Oct 29.
Preclinical and clinical investigation has shown that hippocampal neuronal atrophy and destruction can be observed in patients with depression, and this can be ameliorated with antidepressant medication. Neuroprotection has therefore been proposed as one of the mechanisms of action of antidepressants. Paeoniflorin, a monoterpene glycoside, has been reported to display antidepressant-like effects in animal models of behavioral despair. The present study aimed to examine the protective effect of paeoniflorin treatment on N-methyl-D-aspartate (NMDA)-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. Paeoniflorin was shown to elevate cell viability, decrease lactate dehydrogenase (LDH) release in NMDA-treated PC12 cells. Paeoniflorin also reversed the increased intracellular calcium (Ca(2+)) concentration and the reduced Calbindin-D28K mRNA level caused by NMDA in PC12 cells. These results suggest that paeoniflorin exerts a neuroprotective effect on NMDA-induced neurotoxicity in PC12 cells, at least in part, via Ca(2+) antagonism.
临床前和临床研究表明，抑郁症患者可观察到海马神经元萎缩和破坏，而抗抑郁药物可改善这种情况。因此，神经保护被认为是抗抑郁药的作用机制之一。芍药苷是一种单萜糖苷，已被报道在行为绝望的动物模型中具有抗抑郁样作用。本研究旨在探讨芍药苷治疗对 N-甲基-D-天冬氨酸（NMDA）诱导的培养大鼠嗜铬细胞瘤（PC12）细胞毒性的保护作用。结果表明，芍药苷可提高 NMDA 处理的 PC12 细胞的细胞活力，降低乳酸脱氢酶（LDH）的释放。芍药苷还可逆转 NMDA 引起的 PC12 细胞内钙离子（Ca(2+)）浓度升高和钙结合蛋白 D28K mRNA 水平降低。这些结果表明，芍药苷通过钙拮抗作用对 NMDA 诱导的 PC12 细胞毒性发挥神经保护作用。
