Liu Jing, He Qiao-Jie, Zou Wei, Wang Hong-Xia, Bao Yong-Ming, Liu Yu-Xin, An Li-Jia
Department of Bioscience and Biotechnology, School of Environmental and Biological Sciences, Dalian University of Technology, 2 Linggong Road, Dalian, Liaoning 116024, PR China.
Brain Res. 2006 Dec 6;1123(1):68-79. doi: 10.1016/j.brainres.2006.09.058. Epub 2006 Oct 31.
Rehmannia, a traditional Chinese medical herb, has a long history in age-related disease therapy. Previous work has indicated that catalpol is a main active ingredient performing neuroprotective effect in rehmannia, while the mechanism underlying the effect remains poorly understood. In this study, we attempt to investigate the effect of catalpol on presynaptic proteins and explore a potential mechanism. The hippocampal levels of GAP-43 and synaptophysin in 3 groups of 4 months (young group), 22-24 months (aged group) and catalpol-treated 22-24 months (catalpol-treated group) rats were evaluated by western blotting. Results clearly showed a significant decrease in synaptophysin (46.6%) and GAP-43 (61.4%) levels in the aged group against the young animals and an increase (45.0% and 31.8% respectively) in the catalpol-treated aged rats in comparison with the untreated aged group. In particular, synaptophysin immunoreactivity (OD) in the dentate granule layer of the hippocampus was increased 0.0251 in the catalpol-treated group as compared with the aged group. The study also revealed a catalpol-associated increase of PKC and BDNF in the hippocampus of the catalpol-treated group in comparison with the aged rats and highly correlated with synaptophysin and GAP-43. Such positive correlations between presynaptic proteins and signaling molecules also existed in the young group. These results suggested that catalpol could increase presynaptic proteins and up-regulate relative signaling molecules in the hippocampus of the aged rats. Consequently, it seemed to indicate that catalpol might ameliorate age-related neuroplasticity loss by "normalizing" presynaptic proteins and their relative signaling pathways in the aged rats.
熟地黄，一种传统的中草药，在治疗与年龄相关的疾病方面有着悠久的历史。先前的研究表明，梓醇是熟地黄中发挥神经保护作用的主要活性成分，但其作用机制仍不清楚。在本研究中，我们试图研究梓醇对突触前蛋白的影响，并探索其潜在机制。通过蛋白质免疫印迹法评估了4个月龄（年轻组）、22 - 24个月龄（老年组）以及梓醇处理的22 - 24个月龄（梓醇处理组）三组大鼠海马中GAP - 43和突触素的水平。结果清楚地表明，与年轻动物相比，老年组突触素水平显著降低（46.6%），GAP - 43水平显著降低（61.4%）；与未处理的老年组相比，梓醇处理的老年大鼠中这两种蛋白水平有所升高（分别为45.0%和31.8%）。特别是，与老年组相比，梓醇处理组海马齿状颗粒层中突触素免疫反应性（光密度值）增加了0.0251。该研究还显示，与老年大鼠相比，梓醇处理组大鼠海马中PKC和BDNF增加，且与突触素和GAP - 43高度相关。年轻组中突触前蛋白与信号分子之间也存在这种正相关。这些结果表明，梓醇可以增加老年大鼠海马中的突触前蛋白，并上调相关信号分子。因此，这似乎表明梓醇可能通过“恢复正常”老年大鼠突触前蛋白及其相关信号通路来改善与年龄相关的神经可塑性丧失。
